Nonopsonic FIMH-Mediated phagocytosis of E. coli and its possible contribution to recurrent urinary tract infections

Publisher Summary By binding to the FimH receptor, CD48, nonopsonized E. coli can gain access to a lipid processing pathway that bypasses the normal phagocytic killing mechanisms. Recent studies in the laboratory employing mouse bone marrow-derived mast cells suggest that this mode of phagocytosis may also be observed in other phagocytic cells (unpublished observations). It is also noteworthy that previous work with opsonized, nonopsonized Toxoplasma gondii , and macrophages have reported essentially similar outcomes as that described with E. coli . Although the parasite's adhesin and complementary macrophage receptor are unknown, many features of these interactions resemble those mediated by FimH-expressing bacteria and macrophages including the requirement of oponins to induce intracellular fusion of parasite containing endosome with lysosome or lowering of internal endosome pH. These findings suggest that this mode of opsonin-independent binding and entry of pathogens into phagocytic cells may be a more common mode of pathogenesis than was initially assumed.