Biophysical Society Thematic Meeting | Ascona 2026

PROGRAM & ABSTRACTS

Biophysical Society Thematic Meetings

Mechanobiology of Infection

Ascona, Switzerland | June 7–11, 2026

Organizing Committee

Effie Bastounis, University of Tübingen, Germany Daria Bonazzi, Institut Pasteur, France Alexandre Persat, EPFL, Switzerland

Thank You to Our Sponsors!

Thank you to all sponsors for their support.

Mechanobiology of Infection

Welcome Letter

June 2026

Dear Colleagues, We are delighted to welcome you to the Biophysical Society Thematic Meeting entitled Mechanobiology of Infection, taking place in Ascona, Switzerland, from June 7–11, 2026. This meeting is the first international conference dedicated to the emerging field of the mechanobiology of infection, which lies at the interface of microbiology, biophysics, engineering, and infection biology. The goal of this meeting is to bring together researchers exploring how mechanical forces shape bacterial behavior, host responses, immune defense, and treatment outcomes, while fostering new collaborations across disciplines. Overall, the conference will feature invited lectures, contributed talks, poster sessions, and discussions bringing together scientists from a broad range of backgrounds and expertise. We hope this meeting will not only provide an exciting venue to share recent discoveries, but also stimulate new ideas, collaborations, and long term connections within this rapidly growing community. We warmly encourage all participants to actively engage in the discussions following talks, during poster sessions, and throughout the informal exchanges that will take place during coffee breaks, meals, and social events. We also hope you will enjoy the exceptional setting of Monte Verità and the beautiful region of Ascona. We would like to thank our generous sponsors and institutional supporters for making this meeting possible. The Organizing Committee Effie Bastounis, University of Tübingen, Germany

Daria Bonazzi, Institut Pasteur, France Alexandre Persat, EPFL, Switzerland

Mechanobiology of Infections

Code of Conduct

Biophysical Society Code of Conduct, Anti-Harassment Policy The Biophysical Society (BPS) is committed to providing an environment that encourages the free expression and exchange of scientific ideas. As a global, professional Society, the BPS is committed to the philosophy of equal opportunity and respectful treatment for all, regardless of national or ethnic origin, religion or religious belief, gender, gender identity or expression, race, color, age, marital status, sexual orientation, disabilities, veteran status, or any other reason not related to scientific merit. All BPS meetings and BPS-sponsored activities promote an environment that is free of inappropriate behavior and harassment by or toward all attendees and participants of Society events, including speakers, organizers, students, guests, media, exhibitors, staff, vendors, and other suppliers. BPS expects anyone associated with an official BPS-sponsored event to respect the rules and policies of the Society, the venue, the hotels, and the city. Definition of Harassment The term “harassment” includes but is not limited to epithets, unwelcome slurs, jokes, or verbal, graphic or physical conduct relating to an individual’s race, color, religious creed, sex, national origin, ancestry, citizenship status, age, gender or sexual orientation that denigrate or show hostility or aversion toward an individual or group. Sexual harassment refers to unwelcome sexual advances, requests for sexual favors, and other verbal or physical conduct of a sexual nature. Behavior and language that are welcome/acceptable to one person may be unwelcome/offensive to another. Consequently, individuals must use discretion to ensure that their words and actions communicate respect for others. This is especially important for those in positions of authority since individuals with lower rank or status may be reluctant to express their objections or discomfort regarding unwelcome behavior. It does not refer to occasional compliments of a socially acceptable nature. It refers to behavior that is not welcome, is personally offensive, debilitates morale, and therefore, interferes with work effectiveness. The following are examples of behavior that, when unwelcome, may constitute sexual harassment: sexual flirtations, advances, or propositions; verbal comments or physical actions of a sexual nature; sexually degrading words used to describe an individual; a display of sexually suggestive objects or pictures; sexually explicit jokes; unnecessary touching. Attendees or participants who are asked to stop engaging in harassing behavior are expected to comply immediately. Anyone who feels harassed is encouraged to immediately inform the alleged harasser that the behavior is unwelcome. In many instances, the person is unaware that their conduct is offensive and when so advised can easily and willingly correct the conduct so that it does not reoccur. Anyone who feels harassed is NOT REQUIRED to address the person believed guilty of inappropriate treatment. If the informal discussion with the alleged harasser is unsuccessful in remedying the problem or if the complainant does not feel comfortable with such an approach, they can report the behavior as detailed below. Reported or suspected occurrences of harassment will be promptly and thoroughly investigated. Following an investigation, BPS will immediately take any necessary and appropriate action. BPS will not permit or condone any acts of retaliation against anyone who files harassment complaints or cooperates in the investigation of same. Reporting a Violation Violations of this Conduct Policy should be reported immediately. If you feel physically unsafe or believe a crime has been committed, you should report it to the police immediately. To report a violation to BPS:

• You may do so in person at the Annual Meeting at the BPS Business Office in the convention center.

Mechanobiology of Infections

Code of Conduct

• You may do so in person to BPS senior staff at Thematic Meetings, BPS Conferences, or other BPS events.

• At any time (during or after an event), you can make a report through

http://biophysics.ethicspoint.com or via a dedicated hotline (phone numbers listed on the website) which will collect and relay information in a secure and sensitive manner.

Reported or suspected occurrences of harassment will be promptly and thoroughly investigated per the procedure detailed below. Following an investigation, BPS will immediately take any necessary and appropriate action. BPS will not permit or condone any acts of retaliation against anyone who files harassment complaints or cooperates in the investigation of same. Investigative Procedure All reports of harassment or sexual harassment will be treated seriously. However, absolute confidentiality cannot be promised nor can it be assured. BPS will conduct an investigation of any complaint of harassment or sexual harassment, which may require limited disclosure of pertinent information to certain parties, including the alleged harasser. Once a complaint of harassment or sexual harassment is received, BPS will begin a prompt and thorough investigation. Please note, if a complaint is filed anonymously, BPS may be severely limited in our ability to follow-up on the allegation. • An impartial investigative committee, consisting of the current President, President-Elect, and Executive Officer will be established. If any of these individuals were to be named in an allegation, they would be excluded from the committee. • The committee will interview the complainant and review the written complaint. If no written complaint exists, one will be requested. • The committee will speak to the alleged offender and present the complaint. • The alleged offender will be given the opportunity to address the complaint, with sufficient time to respond to the evidence and bring his/her own evidence. • If the facts are in dispute, the investigative team may need to interview anyone named as witnesses. • The investigative committee may seek BPS Counsel’s advice. • Once the investigation is complete, the committee will report their findings and make recommendations to the Society Officers. • If the severity of the allegation is high, is a possible repeat offense, or is determined to be beyond BPS’s capacity to assess claims and views on either side, BPS may refer the case to the alleged offender’s home institution (Office of Research Integrity of similar), employer, licensing board, or law enforcement for their investigation and decision. Disciplinary Actions Individuals engaging in behavior prohibited by this policy as well as those making allegations of harassment in bad faith will be subject to disciplinary action. Such actions range from a written warning to ejection from the meeting or activity in question without refund of registration fees, being banned from participating in future Society meetings or Society-sponsored activities, being expelled from membership in the Society, and reporting the behavior to their employer or calling the authorities. In the event that the individual is dissatisfied with the results of the investigation, they may appeal to the President of the Society. Any questions regarding this policy should be directed to the BPS Executive Officer or other Society Officer.

Mechanobiology of Infections

Table of Contents

Table of Contents

General Information .............................................................................................................. 1 Program Schedule ................................................................................................................. 3

Speaker Abstracts .................................................................................................................. 9

Poster Sessions ...................................................................................................................... 50

Mechanobiology of Infection

General Information

GENERAL INFORMATION

Registration Location and Hours Registration will take place at the Reception Desk of Monte Verità. Registration will be open continuously from 15:00 on June 7 through 17:00 on June 10. BPS Information Desk Location and Hours BPS Information Desk will be located at the corridor to the Auditorium of Monte Veritá. Hours are as follows: Sunday, June 7 16:00 – 19:00 Monday, June 8 8:30 – 17:00 Tuesday, June 9 8:30 – 12:00 Wednesday, June 10 8:30 – 17:00 Instructions for Presentations (1) Presentation Facilities: A data projector will be made available in the Auditorium. The Monte Veritá will provide one (1) PC laptop and one (1) Macintosh laptop. Speakers who need to run a special program should bring their personal laptop. Speakers are advised to preview their final presentations before the start of each session. (2) Poster Sessions: 1) All poster sessions will be held in Balint Salon. 2) A display board measuring 1189 mm (3’ 10”) high by 841 mm (2’ 9”) wide will be provided for each poster. 3) There will be formal poster presentations on Sunday and Monday. All posters will be available for viewing during all poster sessions. 4) During the assigned poster presentation sessions, presenters are requested to remain in front of their poster boards to meet with attendees. 5) All posters left uncollected at the end of the meeting will be disposed. Note Pads/Pens CSF name tags, CSF bags, BPS and CSF pens and CSF notepads will be provided. Meals and Coffee Breaks There will be a two-hour Welcome Reception on Monday, June 8 from 17:00-19:00. This reception will be held in Sala Balint located on the first floor of the main building. Weather permitting, the terrace in front of Sala Balint is for the exclusive use of the conference participants.

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Mechanobiology of Infection

General Information

Coffee breaks will be served in the Sala Balint as well. Breakfasts, lunches, and dinners will be served in the dining hall, Sala Luce, which is located on the first floor of the main building. Smoking Please be advised that smoking is not permitted inside Monte Veritá or the meeting facilities. Smoking is permitted in outside areas. Name Badges Name badges are required to enter all scientific sessions, poster sessions, and social functions. Please wear your badge throughout the conference. Internet Wi-Fi will be provided at the venue. Information will be available at the registration desk.

Contact Information If you have any further requirements during the meeting, please contact the meeting staff at the

registration desk from June 7-10 during registration hours. In case of emergency, you may contact the following:

Dorothy Chaconas, BPS Staff dchaconas@biophysics.org Umi Zhou, BPS Staff uzhou@biophysics.org Front Desk, Monte Veritá + 41 91 785 40 40

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Program Schedule

Mechanobiology of Infection Ascona, Switzerland June 7-11, 2026 PROGRAM

Sunday, June 7, 2026

16:00 – 19:00

Registration/Information

Reception Desk

17:00 – 17:15

Welcome and Opening Remarks Daria Bonazzi, Institut Pasteur, France

Session I

Mechanics of Bacterial Collectives Chair: Vasily Zaburdaev, University of Erlangen-Nuremberg, Germany Jing Yan, Yale University, USA Single-Cell Imaging of Microbial Communities Across Different Spatial and Temporal Scales Vivek Thacker, Heidelberg University, Germany * Mechanobiology in Tuberculosis: How the Emergent Mechanical Resilience of Cords Influences Infection and Antibiotic Therapy Fan Jin, Shenzhen Institutes of Advanced Technology, China Mechanical Compression Activates Camp Signaling in Pseudomonas Aeruginosa

17:15 – 17:45

17:45 – 18:00

18:00 – 18:30

18:30 – 18:15

Laure Le Blanc, EPFL, Switzerland * Bacteria Tune Collective Navigation by Mechanosensing Collisions

18:15 – 19:00

Flash Poster Talks

19:00 – 20:30

Dinner

Sala Luce

20:30 – 22:00

Poster Session I

Sala Balint

Monday, June 8, 2026

8:30 – 17:00

Registration/Information

Reception Desk

8:45 – 9:00

Welcome Address from CSF

Session II

Mechanics in Host-Microbe Interactions Chair: Effie Bastounis, University of Tübingen, Germany

9:00 – 9:30

Rebecca Lamason, MIT, USA Breaking and Entering: How Rickettsia Forces Its Way Across Cellular Barriers Teuta Pilizota, University of Edinburgh, United Kingdom Mechanical Properties of Escherichia Coli Envelope, and Efforts to Observe These in Infection-Relevant, Host-Like Environments

9:30 – 10:00

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Program Schedule

10:00 – 10:15

Erva Keskin, University of Tübingen, Germany * Shear Priming Decreases Endothelial Cells' Susceptibility to Listeria Monocytogenes Infection, Likely Due to a Decrease in Macropinocytosis Activity

10:15 – 10:45

Coffee Break

Sala Balint

10:45 – 11:15

Carolina Tropini, University of British Columbia, Canada Mechanobiological Consequences of Bowel Prep: Weakened Barriers and Pathogen Translocation Faith Fore, King's College London, United Kingdom * Airway Epithelia Clear Rhinovirus by Extruding Infected Cells at the Cost of Viral Dissemination Megan Chong, University of California, Berkeley, USA * Probing the Contribution of Actin Network Architecture and Cortical Mechanics in Bacterial-Induced Host Cell Fusion Effie Bastounis, Humboldt University of Berlin, Germany Bacterially-Infected Macrophages Promote Biomechanical Alterations in Endothelial Cell Monolayers for Transmigration Navish Wadhwa, Arizona State University, USA Experimental Evolution Reveals Distinct Flagellar Strategies for Enhanced Motility in Complex Environments Gerard Wong, University of California, Los Angeles, USA When Ancients Meet Moderns: Two Contrasting Perspectives on Initial Contact Between Bacteria and Marine Invertebrates Silvio Bianchi, CNR Nanotec, Italy * Torque Transmission Through the Hook and Its Role in Bundling in E. coli Balint Kiss, Semmelweis University, Hungary * Flexible Motion of T7 Bacteriophage Tail Fibers Suggest a Dynamic Viral Infection Mechanism Maté Biro, Garvan Institute of Medical Research, Australia * Mechanobiology of Cytotoxic Lymphocyte Movements and Interactions Lunch Mechanobiology of Motility Chair: Jing Yan, Yale University, USA

11:15 – 11:30

11:30 – 11:45

11:45 – 12:15

12:15 – 14:00

Sala Luce

Session III

14:00 – 14:30

14:30 – 15:00

15:00 – 15:15

15:15 – 15:30

15:30– 15:45

15:45 – 16:15

Flash Poster Talks

16:15 – 17:00

Networking and One-on-One Discussion

Sala Balint Terrace

17:00 – 18:30

Poster Session II

Sala Balint

18:30 – 19:00

Reception and Gathering

Sala Balint Terrace

19:00 – 20:30

Dinner

Sala Luce

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Program Schedule

Tuesday, June 9, 2026 8:30 – 12:00

Registration/Information

Reception Desk

Session IV

Adhesion and Force Sensing Chair: Alex Persat, EPFL, Switzerland

9:00 – 9:30

Joe Sanfilippo, University of Illinois Urbana-Champaign, USA Bacterial Stress Responses and Surface Adhesion in Shear Flow Ashley Nord, Centre national de la recherche scientifique (CNRS), France Probing Spatiotemporal Electrochemical Dynamics on Single Bacterial Cells

9:30 – 10:00

10:00 – 10:30

Coffee Break

Sala Balint

10:30 – 10:45

Sergei Sukharev, University of Maryland, USA * Local Forces in Bacterial Environmental Adaptation

10:45 – 11:00

Rafael Bernardi, Auburn University, USA * Mechanical Stability Drives Adhesion and Virulence Evolution in Staphylococcus Aureus Khalid Salaita, Emory University, USA DNA Force Sensors Reveal the Role of Mechanical Forces in the Adaptive Immune Response

11:00 – 11:30

11:30 – 12:00

Enrique Rojas, New York University, USA Physical Factors Underlying Rod-Shaped Morphogenesis

12:00– 14:00

Lunch

Sala Luce

14:00 – 19:00

Free Time

19:00 – 20:30

Dinner

Sala Luce

Wednesday, June 10, 2026

8:30 – 17:00

Registration/Information

Reception Desk

Session V

Mechanobiology of Bacterial Cell Growth and of the Envelope Chair: Daria Bonazzi, Institut Pasteur, France

9:00 – 9:30

Morgan Delarue, Laboratory for Analysis and Architecture of Systems (LAAS), France Confined Growth Induces Robust Yeast-To-Hyphal Transition in Candida Albicans Bart Hoogenboom, University College London, United Kingdom * Mechanical Forces as A Tool to Decipher Bacterial Resistance and Death

9:30 – 10:00

10:00 – 10:30

Coffee Break

Sala Balint

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Program Schedule

10:30 – 10:45

Andre Körnig, Bruker Nano, Germany * Correlative AFM-Confocal Mechanotyping of the E.coli Envelope

10:45 – 12:00

Panel Discussion: Hopes and Challenges of Interdisciplinary Research

12:00 – 14:00

Lunch

Sala Luce

Session VI

Computation and Modeling in Mechanomicrobiology Chair: Ashley Nord, Centre national de la recherche scientifique (CNRS), France

14:00 – 14:30

Yilin Wu, Chinese University of Hong Kong, China Emergent Mechanics in Bacteria Communities

14:30 – 15:00

Vasily Zaburdaev, University of Erlangen-Nuremberg, Germany Mechanobiology of Bacterial Colonies and Biofilms

15:00 – 15:30

Joshua Shaevitz, Princeton University, USA Collective Behavior and Active Phase Transitions in Motile Bacterial Populations Sandrasegaram Gnanakaran, Los Alamos National Laboratory, USA * Mechanism of Viral Protein-Mediated Membrane Fusion Maria Jose Gómez Benito, University of Zaragoza, Spain * A Hybrid Model of Cell Monolayers: Mapping the Mechanobiology of Infection

15:30 – 15:45

15:45 – 16:00

16:00 – 17:30

Discussion, Closing Remarks and Biophysical Journal Poster Awards

17:30 – 19:00

Networking and One-on-One Discussion

Sala Balint Terrace

19:00 – 20:30

Dinner

Sala Luce

*Contributed talks selected from among submitted abstracts

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Speaker Abstracts

SPEAKER ABSTRACTS

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Sunday Speaker Abstracts

SINGLE-CELL IMAGING OF MICROBIAL COMMUNITIES ACROSS DIFFERENT SPATIAL AND TEMPORAL SCALES Jing Yan Yale University, Molecular, Cellular and Developmental Biology, New Haven, CT, USA Biofilm is an important lifestyle of bacteria where bacterial cells collectively form surface associated aggregates embedded in a polymeric matrix they secrete. Important in industry and medicine, biofilms also represent a unique form of growing active matter with unique physical and material properties. In this talk, I will highlight our recent work on developing a platform for imaging live, growing biofilm at single-cell resolution, using Vibrio cholerae as the model organism. We showed how bacterial cells physically communicate with each other and the environment to form ordered architecture reminiscent of nematic liquid crystals. Moreover, we discovered that heterogeneity in gene expression leads to unexpected pattern formation in biofilm through a drag-based sorting mechanism. I will also highlight ongoing research in the lab on extending the imaging capability to more natural environments including animal hosts. I will end by showing our recent findings on the biophysical properties of the extracellular matrix that underlie the architecture of the biofilm.

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Sunday Speaker Abstracts

MECHANOBIOLOGY IN TUBERCULOSIS: HOW THE EMERGENT MECHANICAL RESILIENCE OF CORDS INFLUENCES INFECTION AND ANTIBIOTIC THERAPY Vivek Thacker 1 ; Richa Mishra 1 ; Anna Rafalik 1 ; Melanie Hannebelle 2 ; 1 Heidelberg University Medical Faculty, Heidelberg, Germany 2 Swiss TPH, Basel, Switzerland Single virulent mycobacteria grow into visually-striking serpentine cords. This defining phenomenological feature was reported decades ago, but we still understand very little about the need for such a highly-ordered structure and why cording is so closely associated with virulence. Using a microphysiological lung-chip model [1] and volumetric imaging of C3HeB/FeJ mouse model tissue, we recently identified mechanical resilience as a defining feature of cords – linking immunosuppression early in infection in susceptible cells, with impact on long-term lesion architecture by facilitating dissemination, tissue damage, and necrosis [2]. Additionally, cords also harbour antibiotic tolerant bacteria, including in animal models. I will describe recent work towards understanding interbacterial interactions in cords, their biophysical implications, and approaches to target this via host-directed therapy in TB. 1. Mishra & Hannebelle et al., Cell, 2023, 186(e28), 5135-5150. 2. Thacker et al., eLife, 2019. Doi: 10.7554/elife.59961.

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Sunday Speaker Abstracts

MECHANICAL COMPRESSION ACTIVATES CAMP SIGNALING IN PSEUDOMONAS AERUGINOSA Fan Jin ; Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China In Pseudomonas aeruginosa, cyclic AMP (cAMP) is a critical regulator of the type III secretion system (T3SS), whose abundance directly impacts bacterial virulence. Yet, the environmental signals that activate cAMP signaling remain incompletely understood. Here, using the real-time cAMP biosensor Gflamp1, we demonstrate that mechanical compression triggers cAMP elevation in P. aeruginosa. Combining microfluidics, image processing, and physical modelling, we estimated a mechanical force threshold of ~30 nN for cAMP activation. Genetic studies revealed that this mechanoresponse depends on the Pil-Chp chemotaxis system and the FimV FimL complex, along with the adenylate cyclase CyaB, but does not require surface-exposed type IV pili. We demonstrated direct interaction between the histidine kinase ChpA and the polar scaffolding protein FimV, and that FimL competes with ChpA for FimV binding. FRET-FLIM analysis indicated that ChpA moves closer to both PilG and FimL under mechanical compression. We further showed global upregulation of T3SS-associated genes during compressed-state bacterial growth. These findings offer insights into the dynamic processes underlying bacterial infection in host organisms.

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Sunday Speaker Abstracts

BACTERIA TUNE COLLECTIVE NAVIGATION BY MECHANOSENSING COLLISIONS Laure Le Blanc 1,2 ; Giona Cattaneo 1,2 ; Nathel Heraud 1,2 ; Einollah Sarikhani 3 ; Dhivya Pushpa Meganathan 3 ; Chia-Ni Tsai 1,2 ; Anum Tahir 3 ; Marco Kühn 1,2 ; Zeinab Jahed 3 ; Sangwoo Kim 4 ; Alexandre Persat 1,2 ; 1 École Polytechnique Fédérale de Lausanne, Global Health Institute, School of Life Sciences, Lausanne, Switzerland 2 École Polytechnique Fédérale de Lausanne, Institute of Bioengineering, School of Life Sciences, Lausanne, Switzerland 3 University of California San Diego, Department of Chemical and Nano Engineering, La Jolla, CA, USA 4 École Polytechnique Fédérale de Lausanne, Institute of Mechanical Engineering, Lausanne, Switzerland Navigating complex environments is a fundamental challenge shared across the tree of life, requiring organisms to balance individual and collective locomotion. Here, we show that the bacterial pathogen Pseudomonas aeruginosa balance individual and group motility using mechanosensation to enhance surface exploration. During twitching motility, P. aeruginosa reverses direction when colliding with neighboring cells, which suppresses the spontaneous group formation characteristic of collective locomotion. Unlike non-reversing mechanosensing mutants that move in cohesive, quasi-ballistic groups, wild-type cells adjust their trajectories with local cell density, transitioning from superdiffusive motion in crowds to quasi-ballistic movement toward new territory. Using microfabricated mazes, we demonstrate that this adaptive behavior enables bacteria to navigate spatially structured environments. We propose that the same principle extends to the colony scale: by continuously reorienting away from the crowd, wild-type cells spread faster than mechanosensing-deficient mutants. Together, these findings establish mechanosensation as a primary driver of the spreading capacity of P. aeruginosa. Given that bacteria must navigate the spatially complex architecture of the lung to establish infection, this mechanosensory strategy may shape early infection dynamics and pathogenesis.

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Monday Speaker Abstracts

BREAKING AND ENTERING: HOW RICKETTSIA FORCES ITS WAY ACROSS CELLULAR BARRIERS Hannah Margolis; Rebecca Lamason Massachusetts Institute of Technology, Cambridge, MA, USA Eukaryotic membranes form formidable barriers that compartmentalize cellular processes, yet some pathogens have evolved mechanisms to breach them and access highly protected intracellular spaces. Here, we investigate the obligate intracellular pathogen Rickettsia parkeri, which undergoes a complex and dynamic intracellular lifecycle unlike that of many human pathogens. A particularly striking feature of this lifecycle is its unusually frequent invasion of human nuclei. Using live-cell and fixed-cell microscopy, we found that R. parkeri harnesses actin-based motility to drive into the nuclear envelope and generate extensive protrusions that support both nuclear entry and exit without causing overt damage to the host cell. To identify factors that mediate this process, we applied a proteomic labeling approach and discovered novel secreted effectors, including one that specifically localizes to sites of nuclear invasion and egress. Loss of this effector reduced successful nuclear invasion while increasing caspase activation and subsequent host cell death. Together, these findings reveal an unexpected capacity of R. parkeri to forcibly access intracellular spaces typically considered inaccessible and underscore the need to understand how this remarkable adaptation evolved.

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Monday Speaker Abstracts

MECHANICAL PROPERTIES OF ESCHERICHIA COLI ENVELOPE, AND EFFORTS TO OBSERVE THESE IN INFECTION-RELEVANT, HOST-LIKE INVIRONMENTS Teuta Pilizota ; Saheli Mitra; Smitha Hegde; Pietro Cicuta University of Cambridge, Department of Physics, Cambrdige, United Kingdom A bacterial cell envelope is a unique active material whose mechanical properties are arguably not yet understood despite decades of active research. To decipher how the cell envelope dissipates energy and resists deformation, we place individual Escherichia coli cells under constant, long-term volumetric strain. For the purpose, we created an E.coli mutant with deletion of its seven mechanosensitive channels, and we demonstrate that under hypoosmotic downshocks of increasing magnitudes, the average cell volume increases and does not recover the characteristic response of the wild type. After a few hours of sustained volume expansion cells exhibit delayed-lysis and slow plastic deformation. We propose a mathematical model of the time-dependent response of dying cells to constant, high volumetric strain caused by the downshocks that describes the mechanical properties of the E.coli envelope. Next, we wish to study cell envelope mechanics that resemble sinus environment of a human host. Such environment is ripe with multi-scale interactions, and numerous physical and biological factors involved. We show our efforts to mimic such environment through maintaining epithelial cells under constant flow under a microscope and to characterise the rheological properities of such environment, all before we introduce bacterial cells to it.

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Monday Speaker Abstracts

SHEAR PRIMING DECREASES ENDOTHELIAL CELLS' SUSCEPTIBILITY TO LISTERIA MONOCYTOGENES INFECTION, LIKELY DUE TO A DECREASE IN MACROPINOCYTOSIS ACTIVITY Erva Keskin 1,2 ; Aylin Balmes 3 ; Julio Cesar Sanchez-Rendon 1,2 ; Mai Wang 4 ; Tilman Schäffer 3 ; Effie Bastounis 1,2 ; 1 University of Tübingen, Interfaculty Institute of Microbiology and Infection Medicine, Cluster of Excellence "Controlling Microbes to Fight Infections" (CMFI, EXC 2124), Tübingen, Germany 2 Humboldt-University of Berlin, Institute for Biology, Berlin, Germany 3 University of Tübingen, Institute for Applied Physics, Tübingen, Germany 4 University Hospital Heidelberg, Medical Microbiology and Hygiene, Heidelberg, Germany Endothelial cells (ECs) form a protective barrier lining blood vessels, yet blood-borne pathogens such as Listeria monocytogenes (Lm) can breach this interface to cause systemic infection. While host-pathogen biochemical interactions are well studied, how mechanical forces generated by blood flow regulate endothelial susceptibility to infection remains poorly understood. We hypothesized that shear stress mechanically primes ECs by increasing cortical tension, thereby suppressing endocytic uptake pathways exploited by Lm.To test this, we applied controlled apical shear stress gradients to EC monolayers using a fluid jet device and quantified bacterial infection rate, adhesion and invasion after flow was stopped. Shear-exposed ECs exhibited a significant reduction in Lm internalization compared to monolayers never exposed to flow (static conditions). This decreased susceptibility extended to non-pathogenic Listeria innocua indicating a general suppression of passive uptake rather than pathogen-specific signaling. Atomic force microscopy (AFM) revealed a significant increase in cortical stiffness in shear-primed ECs and TFM measurements showed elevated traction stresses under flow exposure, indicating elevated membrane tension. Functionally, pharmacological inhibition or nutrient starvation-induced suppression of macropinocytosis phenocopied the shear-induced protection, significantly reducing bacterial entry under static conditions. These findings support a model in which Lm exploits macropinocytic pathways for endothelial entry that are mechanically inhibited by shear stress. Together, our results identify shear-dependent mechanical regulation of macropinocytosis as a key determinant of endothelial susceptibility to Lm infection and suggest that vascular regions experiencing disturbed or low shear stress may represent invasion hot spots.

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Monday Speaker Abstracts

MECHANOBIOLOGICAL CONSEQUENCES OF BOWEL PREP: WEAKENED BARRIERS AND PATHOGEN TRANSLOCATION Carolina Tropini University of British Columbia, Vancouver, BC, Canada Mechanical forces and physicochemical parameters within the gut are central regulators of host– microbe interactions, yet clinical procedures that acutely perturb this environment are rarely examined through a mechanobiological lens. Bowel preparation (BP), an osmotic laxative regimen routinely administered prior to colonoscopy, induces rapid fluid shifts and mechanical clearance of luminal contents. Despite its widespread use, its impact on mucosal barrier mechanics and susceptibility to infection has remained poorly defined. Using reductionist mouse models, humanized microbiota systems, and in vitro approaches, we demonstrate that polyethylene glycol–based BP constitutes a transient but profound biomechanical disruption of the gut ecosystem. Within hours, BP increases luminal osmolality, depletes short-chain fatty acids, and decimates the mucus layer, reducing both its thickness and epithelial coverage. These changes occur without overt epithelial damage yet significantly weaken colonization resistance. Under these mechanically altered conditions, Salmonella enterica serovar Typhimurium robustly colonizes the gut in the absence of antibiotics, including non-motile mutants typically impaired in invasion. BP further facilitates pathogen translocation to mesenteric lymph nodes, liver, and spleen, and exacerbates inflammation in a chemically induced colitis model. Mechanistically, our findings suggest that osmotic stress and mucus depletion together reshape the physical landscape that constrains microbial access to the epithelium. By transiently altering barrier mechanics, nutrient availability, and spatial organization, BP lowers the threshold for pathogen establishment and systemic dissemination. These results position bowel preparation as a clinically relevant model of acute biomechanical perturbation, revealing how short-lived shifts in tissue mechanics and luminal environment can have outsized consequences for infection biology. More broadly, this work underscores the importance of integrating mechanical and biophysical parameters into our understanding of host–pathogen interactions, particularly in vulnerable populations such as individuals with inflammatory bowel disease.

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Mechanobiology of Infection

Monday Speaker Abstracts

AIRWAY EPITHELIA CLEAR RHINOVIRUS BY EXTRUDING INFECTED CELLS AT THE COST OF VIRAL DISSEMINATION Faith Fore 1,2 ; Dustin C Bagley 1,2 ; Rocio T Martinez-Nunez 3 ; Julia Aniscenko 4 ; Sebastian Johnston 4 ; Jody Rosenblatt 1,2 ; 1 King's College London, Randall Centre for Cell and Molecular Biophysics, London, United Kingdom 2 The Francis Crick Institute, London, United Kingdom 3 King's College London, Infectious Diseases, London, United Kingdom 4 Imperial College London, National Heart and Lung Institute, London, United Kingdom Rhinoviruses (RV), the primary cause of the common cold and a major trigger of asthma exacerbations and related hospitalisations, predominantly infect airway epithelia. These tissues maintain barrier integrity by removing damaged or excess cells through cell extrusion, a conserved homeostatic mechanism. While extrusion can eliminate infected cells, some pathogens exploit this process to facilitate dissemination. Here, we show that RV-infected cells are selectively extruded from airway epithelia, reducing viral burden to ~4% within 24 hours. We term this process virus-induced cell extrusion (VICE), a barrier-dependent mechanism observed in both 16HBE14o ⁻ bronchial monolayers and fully differentiated primary human airway epithelia. In contrast, BEAS-2B cells, which fail to form tight monolayers, cannot eliminate infected cells and instead accumulate viral burden, underscoring the importance of epithelial architecture in antiviral defence. VICE proceeds in two distinct waves. An early, non-apoptotic phase is driven by stretch-activated channels (SACs), as demonstrated by sensitivity to SAC inhibitors (Gd³ ⁺ , GsMtx4), and occurs prior to complete viral internalisation, independent of dynamin-mediated endocytosis. A later apoptotic phase depends on viral replication. Both phases require sphingosine-1-phosphate (S1P) signalling through the S1P2 receptor, identifying S1P as a central regulator of extrusion during infection. Despite promoting viral clearance, extrusion expels viable, virus-laden cells that remain infectious and can initiate infection in naïve epithelia. Thus, VICE acts as a cell-intrinsic, leukocyte-independent mechanism that rapidly removes infected cells while increasing the potential for viral dissemination to new hosts. Together, these findings redefine airway epithelia as active drivers of antiviral defence and reveal a fundamental trade-off between pathogen clearance and transmission.

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Mechanobiology of Infection

Monday Speaker Abstracts

PROBING THE CONTRIBUTION OF ACTIN NETWORK ARCHITECTURE AND CORTICAL MECHANICS IN BACTERIAL-INDUCED HOST CELL FUSION Megan K Chong ; Matthew D Welch University of California, Berkeley, Molecular & Cell Biology, Berkeley, CA, USA Bacteria from the pseudomallei group of Burkholderia species, a group of Gram-negative, facultative intracellular bacteria, spread by inducing host cell-cell fusion to form multinucleate giant cells. Host cell fusion relies on the polymerization of actin at the bacterial surface, generating an actin network, and driving actin-based motility. When moving bacteria collide with the plasma membrane, bacteria extend into plasma-membrane protrusions that push into neighboring cells. Fusion occurs within these protrusions, but it remains unclear what molecular and mechanical mechanisms mediate this cell-cell fusion and spread. Specifically, how distinct actin network architectures impact protrusion extension dynamics and host cell fusion efficiency, and whether host cell mechanics (e.g. membrane and cortical tension) promote or constrain cell cell fusion, are not known. Here, we use live-cell imaging to compare dynamics between bacteria expressing actin-based motility effectors from different Burkholderia species. We find that bacterial force generation depends on actin network architecture, with branched Arp2/3-mediated actin networks extending protrusions significantly faster and farther and undergoing fewer reversals than bundled actin networks generated via an Ena/VASP-like mechanism. Additionally, reducing host cell cortical contractility by myosin II inhibition leads to more processive movement of bacteria within protrusions and longer protrusions for bacteria that polymerize bundled but not branched actin networks. This suggests an active interplay between the actin mediated forces generating protrusions and the resistive forces at the host cell boundary that may determine the rate of bacterial induced cell-cell fusion. Ongoing experiments will measure how protrusion dynamics impact cell-cell fusion, and how membrane tension changes in response to protrusions. This work will provide a framework for how Burkholderia species hijack underlying host cell biology to mediate infections and how mammalian cell mechanics and molecular co factors both promote and constrain cell-cell fusion and bacterial spread.

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Mechanobiology of Infection

Monday Speaker Abstracts

BACTERIALLY-INFECTED MACROPHAGES PROMOTE BIOMECHANICAL ALTERATIONS IN ENDOTHELIAL CELL MONOLAYERS FOR TRANSMIGRATION Effie Bastounis Humboldt University of Berlin, Germany

No Abstract

EXPERIMENTAL EVOLUTION REVEALS DISTINCT FLAGELLAR STRATEGIES FOR ENHANCED MOTILITY IN COMPLEX ENVIRONMENTS Seiga Yanagisawa 1,2 ; Wayne D Frasch 3 ; Navish Wadhwa 1,2,4 ; 1 Arizona State University, Biodesign Center for Mechanisms of Evolution, Tempe, AZ, USA 2 Arizona State University, Center for Biological Physics, Tempe, AZ, USA 3 Arizona State University, School of Life Sciences, Tempe, AZ, USA 4 Arizona State University, Department of Physics, Tempe, AZ, USA Bacterial pathogens must navigate the complex, viscous environments of host tissues to establish infection, yet how bacteria tune their flagellar machinery to optimize motility in such environments remains an open question. Using experimental evolution, we show that E. coli rapidly evolves enhanced motility in structured media through two distinct strategies: increasing flagella number and altering the shape of the flagellar filament. Strikingly, these changes do not always translate to faster swimming in liquid, revealing that motility in structured environments is mechanistically distinct from swimming in bulk fluid. By tracing this altered filament shape to a single point mutation in the flagellin protein FliC, we identify a structural switch within FliC that controls the shape of the filament and, consequently, how well bacteria move through structured environments. These findings reveal how the physical properties of the environment shape the evolution of flagellar function, with implications for understanding how pathogens navigate host tissues during infection.

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Mechanobiology of Infection

Monday Speaker Abstracts

WHEN ANCIENTS MEET MODERNS: TWO CONTRASTING PERSPECTIVES ON INITIAL CONTACT BETWEEN BACTERIA AND MARINE INVERTEBRATES Gerard Wong University of California, Los Angeles, USA

No Abstract

TORQUE TRANSMISSION THROUGH THE HOOK AND ITS ROLE IN BUNDLING IN E. COLI Silvio Bianchi ; Filippo Saglimbeni 1 ; Giacomo Frangipane 2 ; Maria Cristina Cannarsa 2 ; Roberto Di Leonardo 2 ;

1 CNR-NANOTEC, Soft and Living Matter, Rome, Italy 2 Sapienza University of Rome, Physics, Rome, Italy

In Escherichia coli, flagellar motors drive the rotation of helical flagella, enabling propulsion. The torque is transmitted through a deformable, flexible hook that serves as the joint between the motor and the flagellum. This torque transfer mechanism has often been oversimplified or overlooked in previous models. Here, we investigate the intricate dynamics of torque transmission by observing both the rotation/precession of flagella and the motion of an attached micron-sized load using fluorescently labeled flagella. By employing optical tweezers and microfabrication to control bacterial body motion, we demonstrate that the flexibility of the hook and the torque transfer process are critical for the alignment of the flagella.

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Mechanobiology of Infection

Monday Speaker Abstracts

FLEXIBLE MOTION OF T7 BACTERIOPHAGE TAIL FIBERS SUGGEST A DYNAMIC VIRAL INFECTION MECHANISM Luca Elizabet Kosik 1,4 ; Miklós Cervenak 1 ; Dominik Sziklai 1 ; Andrea Balogh-Molnár 1 ; Negar Rahimi 1,5 ; Bence Fehér 1,5 ; Soma Yamamoto 2 ; Hiroki Konno 2 ; Noriyuki Kodera 2 ; Holger Flechsig 2 ; Romain Amyot 2 ; Heinz Amenitsch 3 ; Hedvig Tordai 1 ; Levente Herényi 1 ; Miklós Kellermayer 1,4 ; Balint Kiss 1,4 ; 1 Semmelweis University, Biophysics and Radiation Biology, Budapest, Hungary 2 Kanazawa University, NanoLSI, Kanazawa, Japan Viruses are nanoscale infectious agents capable of specifically targeting and reprograming host cells. A unique group of viruses, bacteriophages, have regained popularity in research partly due to the rising number of multidrug-resistant bacterial infections. Phages could potentially replace antibiotics, but only if we understand every detail of their structure and infection cycle. T7 bacteriophages are a group of dsDNA viruses, which infect E. coli bacteria by recognizing their surface lipopolysaccharides (LPS). T7 virions are comprised of an icosahedral protein shell which encapsulates the genomic DNA, and a tail-fiber complex which is primarily used for target recognition and DNA injection. The virus has six” L”-shaped, ~40 nm long fibers (gp17 protein trimers) attached to the tail-tube, which are thought to be essential for initial host recognition and possibly surface exploration. Using high-speed atomic force microscopy (HS AFM) we observed the molecular structure and movements of isolated tail fibers and the dynamics of fiber to LPS binding. Firstly, we have identified a hinge region within the fibers, which makes them highly flexible, allowing the bending of their distal region. Furthermore, we have observed the dynamic triple helical coiled coil structure of the proximal region, which would allow fiber rotation. These two points of flexibility allow a more efficient and highly dynamic host recognition and virus anchoring process. The observed flexibility might allow host surface exploration by walking. Such flexibility in the host recognition machinery may not be unique to T7 bacteriophages, getting us one step closer to understanding the intricate details of virus-host interactions. 3 Graz University of Technology, Inorganic Chemistry, Graz, Austria 4 HUN-REN-SE, Biophysical Virology Group, Budapest, Hungary 5 HUN-REN, Nanobiophysics Research Group, Budapest, Hungary

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Mechanobiology of Infection

Monday Speaker Abstracts

MECHANOBIOLOGY OF CYTOTOXIC LYMPHOCYTE MOVEMENTS AND INTERACTIONS Maté Biro 1,2 ; 1 Garvan Institute of Medical Research, Sydney, Australia 2 University of New South Wales, Sydney, Australia Cytotoxic lymphocytes can migrate rapidly and with striking versatility in a continuous search for cells to subdue. The mechanisms and cellular forces that underpin the movements and coordinated interactions of T cells and Natural Killer cells are incompletely understood. Here, we investigate the intercellular signalling and mechanical forces that these killer immune cells employ to effectively navigate and converge in 3-dimensional tissues. Using an integrative and multidisciplinary method encompassing cell biology, immunology, 3D live-cell traction-force microscopy, image analysis, optogenetics, biophysics, and modelling, we are uncovering the intricate forces, movements, and interactions exhibited by cytotoxic lymphocytes.

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Mechanobiology of Infection

Tuesday Speaker Abstracts

BACTERIAL STRESS RESPONSES AND SURFACE ADHESION IN SHEAR FLOW Joseph Sanfilippo University of Illinois, Biochemistry, Urbana, IL, USA My research group combines traditional molecular biology approaches with microfluidic technology to examine how host-relevant shear flow impacts stress responses and surface adhesion of the human pathogen Pseudomonas aeruginosa. While reductionist experimental systems provide great mechanistic insight, they commonly lack key aspects of natural systems, such as fluid flow. Thus, there is a great opportunity to solve outstanding problems in microbiology by implementing experimental systems that more precisely model natural conditions. Two major recent discoveries from my lab highlight the scientific opportunities of studying bacteria in flow. First, we discovered that flow sensitizes P. aeruginosa to host-relevant doses of hydrogen peroxide (H 2 O 2 ). Second, we discovered that host-relevant shear forces enhance P. aeruginosa adhesion by counteracting pilus-driven surface departure. Together, these discoveries highlight how using microfluidics can capture bacterial behavior that classical approaches overlook, often revealing unexpected and counterintuitive outcomes.

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Mechanobiology of Infection

Tuesday Speaker Abstracts

PROBING SPATIOTEMPORAL ELECTROCHEMICAL DYNAMICS ON SINGLE BACTERIAL CELLS Anaïs Biquet-Bisquert 1 ; Baptiste Carrio 1 ; Nathan Meyer 1 ; Thales Fernandes 1 ; Manouk Abkarian 1 ; Farida Seduk 2 ; Axel Magalon 2 ; Ashley L Nord ; Francesco Pedaci 1 ; 1 Centre de Biologie Structurale, Université de Mont- pellier, CNRS, INSERM, Montpellier, France 2 Aix Marseille Université, CNRS, Laboratoire de Chimie Bactérienne (UMR7283), IMM, IM2B,, Marseille, France Electrochemical gradients across biological membranes are fundamental to cellular bioenergetics. In bacteria, the proton motive force (PMF) drives critical functions such as ATP synthesis and motility. Although historically regarded as temporally and spatially stable, recent studies have revealed dynamic PMF behaviors at single-cell and community levels, which are implicated in processes like intracellular communication and coordination. The bacterial flagellar motor, a rotary nanomachine directly powered by the PMF, provides a unique and sensitive tool for probing these dynamics. By employing light-activated proton pumps and monitoring changes in flagellar motor activity, we perturb and investigate the PMF at the single-cell level. This approach reveals millisecond-scale temporal fluctuations and rapid lateral homogenization of the PMF, reminiscent of the electrotonic potential spread observed in passive neurons.

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Mechanobiology of Infection

Tuesday Speaker Abstracts

LOCAL FORCES IN BACTERIAL ENVIRONMENTAL ADAPTATION Sergei I. Sukharev ; Elissa Moller; Andriy Anishkin University of Maryland, Biology, College Park, MD, USA

Freshwater is the primary transmission route for enteric pathogens and commensals, requiring robust adaptation to external osmolarity drops. To endure this drastic environmental shift, bacteria rapidly eject small metabolites via tension-activated inner-membrane channels, MscS and MscL, which are present in high numbers (~10^3 per cell). Because MscS is a highly conductive, low-tension-activated channel, a single opening risks instantly de-energizing the cell. How does this align with Δμ H+-based bacterial energetics? We propose that the activity of the MscS population is tightly regulated. During steady growth, most channels stay in a tension insensitive inactivated state but can be reactivated during osmotic shock to release osmolytes. (1) We have shown that the commonly observed splayed conformation of MscS is the inactivated state, stabilized by intercalating lipids separating the peripheral and central helices that form the gate. (2) Computational modeling predicts that the tension-receiving helices can be reconnected to the gate by applying turgor pressure (normal to the membrane), which pushes the gate toward the periplasm, expels lipids, and compacts the structure. (3) Independent analysis of light scattering traces from rapid-dilution experiments on bacterial suspensions indicated that, due to excess inner-membrane area, cells swell significantly (about twofold) before tension reaches the activation threshold for the channels. Given the peptidoglycan expansion modulus, turgor at this point rises to 8-12 atm, which could be sufficient to re-sensitize the inactivated MscS population. (4) After extensive solute release, the total cell volume decreases, increasing cytoplasmic macromolecular crowding that immediately inactivates MscS and terminates the permeability response. Therefore, the adaptive cycle of MscS tracks the sequential changes in local mechanical stress: a surge in turgor recharges the channels and prepares them to respond to tension. As a result, the entire MscS population can remain safely in a tension-insensitive state until osmotic shock occurs.

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