rangkuman demam ISK.docx
description
Transcript of rangkuman demam ISK.docx
Inasymptomatic carriers, the mucosa remains inert,despite the presence of large bacterial numbers in thelumen. Conversely, in acute pyelonephritis, both localand systemic inflammatory response pathways areactivated.
P fimbriae andtype 1 fimbriae use different receptors and different TLR4 signalling pathways. P fimbriae bind to the Gala1-4Galb receptorepitope in the globoseries of glycosphingolipids (GSLs) and activate epithelial cells through TLR4 in an LPS-independent, Ser/Thrprotein kinases-dependent manner and by the release of ceramide. Type 1 fimbriae bind mannose residues (aMan) on glycoproteinsand also activate epithelial cells through TLR4, but with the involvement of a tyrosine protein kinase and LPS.
In epidemiological studies, P fimbriae have shownthe strongest association with acute disease severity,with at least 90% of acute pyelonephritis but less then20% of ABU strains expressing this phenotype
This is in contrast to type 1 fimbriae whichcan be expressed by more than 90% of commensal anduropathogenic E. Coli
P fimbriatedbacteria trigger a significant host response in the murineurinary tract (Linder et al., 1988, 1991). The response isprimarily innate rather than specific, and involves theactivation of chemokines and the recruitment ofneutrophils
P fimbriae promotebacterial persistence and enhance the mucosal hostresponse, while type 1 fimbriae do not appear toinfluence the establishment of bacteriuria or trigger amucosal host response in the human urinary tract in thisway.