Structural highlights
Function
[ESIB_ECOL6] Upon host (human neutrophil) infection interferes with productive FCAR signaling, inhibiting secreted IgA (SIgA) effector functions and probably avoiding neutrophil activation. Inhibits the SIgA-mediated oxidative burst by neutrophils, decreases generation of ROS (reactive oxygen species) by neutrophils and reduces chemotaxis by neutrophils, all of which are SIgA effector functions used to stimulate the immune response. Does not block SIgA-binding to its receptor (FCAR) on neutrophils, but it decreases SIgA-stimulated phosphorylation of cytoplasmic proteins, including phospholipase C-gamma and MAP kinases, all actions that may be advantageous to the pathogen.[1]
References
- ↑ Pastorello I, Rossi Paccani S, Rosini R, Mattera R, Ferrer Navarro M, Urosev D, Nesta B, Lo Surdo P, Del Vecchio M, Rippa V, Bertoldi I, Gomes Moriel D, Laarman AJ, van Strijp JA, Daura X, Pizza M, Serino L, Soriani M. EsiB, a novel pathogenic Escherichia coli secretory immunoglobulin A-binding protein impairing neutrophil activation. mBio. 2013 Jul 23;4(4). pii: mBio.00206-13. doi: 10.1128/mBio.00206-13. PMID:23882011 doi:http://dx.doi.org/10.1128/mBio.00206-13
