DPG Phi
Verhandlungen
Verhandlungen
DPG

Dresden 2014 – scientific programme

Parts | Days | Selection | Search | Updates | Downloads | Help

BP: Fachverband Biologische Physik

BP 7: Posters: Cell adhesion, mechanics and migration

BP 7.8: Poster

Monday, March 31, 2014, 17:30–19:30, P3

Cell mechanics and innate immunity link up during infections — •Andrew Ekpenyong1,3, Si Ming Man2, Sarra Achouri1, Gilbert Ng1,3, Kate Hughes2, Panagiotis Tourlomousis2, John Wright2, Pietro Cicuta1, Clare Bryant2, and Jochen Guck1,31Cavendish Lab., Dept. of Physics, Univ. of Cambridge, UK — 2Dept. of Vet. Medicine, Univ. of Cambridge, UK — 3Biotech. Center, Technische Universität Dresden, Germany.

Infections, in which pathogens invade and colonize host cells, constitute some of the most serious diseases faced by humans. Host cells use immune system proteins and other molecules to fight viral and bacterial invaders. The mechanisms by which these proteins enable cells to survive infections remain unclear. Moreover, during infections, some immune system proteins are known to alter the cytoskeleton, the structure that largely determines cellular mechanical properties. We therefore used an optical stretcher to measure the mechanical properties of primary immune cells (macrophages) during bacterial infection. We found that macrophages become stiffer upon infection. Remarkably, macrophages lacking the proteins, Caspase 1 and NLRC4, lost the stiffening response to infection. This in vitro result correlates with our in vivo data whereby mice lacking Caspase 1 and NLRC4 have more lesions, implying increased bacterial spread. Thus, the immune-protein-dependent increase in cell stiffness in response to bacterial infection seems to have a functional role in the system level fight against pathogens. We will discuss how this functional link between cell mechanics and innate immunity reduces the spread of infection.

100% | Mobile Layout | Deutsche Version | Contact/Imprint/Privacy
DPG-Physik > DPG-Verhandlungen > 2014 > Dresden