ERK activation waves coordinate mechanical cell competition leading to collective elimination via extrusion of bacterially infected cells.

Epithelial cells respond to infection with the intracellular bacterial pathogen Listeria monocytogenes by altering their mechanics to promote collective infected cell extrusion (CICE) and limit infection spread across cell monolayers. However, the underlying biochemical pathways remain elusive. Here, using in vitro (epithelial monolayers) and in vivo (zebrafish larvae) models of infection with L.

StretchView - A Multi-Axial Cell-Stretching Device for Long-Term Automated Videomicroscopy of Living Cells.

Incorporating mechanical stretching of cells in tissue culture is crucial for mimicking (patho)-physiological conditions and understanding the mechanobiological responses of cells, which can have significant implications in areas like tissue engineering and regenerative medicine. Despite the growing interest, most available cell-stretching devices are not compatible with automated live-cell imaging, indispensable for characterizing alterations in the dynamics of various important cellular processes. In this work, StretchView is presented, a multi-axial cell-stretching platform compatible with automated, time-resolved live-cell imaging.

Hybrid model to simulate host cell biomechanics and infection spread during intracellular infection of epithelial monolayers.

Mechanical signals are crucial in regulating the response of cells in a monolayer to both physiological and pathological stressors, including intracellular bacterial infections. In particular, during intracellular infection of epithelial cells in monolayer with the food-borne bacterial pathogen Listeria monocytogenes, cellular biomechanics dictates the degree of bacterial dissemination across the monolayer. This occurs through a process whereby surrounder uninfected cells mechanically compete and eventually extrude infected cells.

P66 is a bacterial mimic of CD47 that binds the anti-phagocytic receptor SIRPα and facilitates macrophage evasion by .

Innate immunity, the first line of defense against pathogens, relies on efficient elimination of invading agents by phagocytes. In the co-evolution of host and pathogen, pathogens developed mechanisms to dampen and evade phagocytic clearance. Here, we report that bacterial pathogens can evade clearance by macrophages through mimicry at the mammalian anti-phagocytic "don't eat me" signaling axis between CD47 (ligand) and SIRPα (receptor).

Keratinocytes use FPR2 to detect and initiate antimicrobial skin defense.

Introduction: Keratinocytes form a multilayer barrier that protects the skin from invaders or injuries. The barrier function of keratinocytes is in part mediated by the production of inflammatory modulators that promote immune responses and wound healing. Skin commensals and pathogens such as secrete high amounts of phenol-soluble modulin (PSM) peptides, agonists of formyl-peptide receptor 2 (FPR2).