rangkuman demam ISK.docx

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In asymptomatic carriers, the mucosa remains inert, despite the presence of large bacterial numbers in the lumen. Conversely, in acute pyelonephritis, both local and systemic inflammatory response pathways are activated. P fimbriae and type 1 fimbriae use different receptors and different TLR4 signalling pathways. P fimbriae bind to the Gala1-4Galb receptor epitope in the globoseries of glycosphingolipids (GSLs) and activate epithelial cells through TLR4 in an LPS-independent, Ser/Thr protein kinases-dependent manner and by the release of ceramide. Type 1 fimbriae bind mannose residues (aMan) on glycoproteins and also activate epithelial cells through TLR4, but with the involvement of a tyrosine protein kinase and LPS. In epidemiological studies, P fimbriae have shown the strongest association with acute disease severity, with at least 90% of acute pyelonephritis but less then 20% of ABU strains expressing this phenotype This is in contrast to type 1 fimbriae which can be expressed by more than 90% of commensal and uropathogenic E. Coli P fimbriated bacteria trigger a significant host response in the murine urinary tract (Linder et al., 1988, 1991). The response is primarily innate rather than specific, and involves the activation of chemokines and the recruitment of neutrophils P fimbriae promote bacterial persistence and enhance the mucosal host response, while type 1 fimbriae do not appear to influence the establishment of bacteriuria or trigger a mucosal host response in the human urinary tract in this way.

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Transcript of rangkuman demam ISK.docx

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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.