MAST-CELL DEGRANULATION INDUCED BY TYPE-1 FIMBRIATED ESCHERICHIA-COLIIN MICE

The strategic location of mast cells at the host-environment interface and their ability to release potent mediators of inflammation have su ggested that these cells may play a pivotal role in host defense again st bacterial infection. The ability of the opportunistic pathogen, Esc herichia coli, to induce degranulation of mast cells obtained from the mouse peritoneum was investigated. We determined that unlike a mutant derivative deficient in the FimH subunit of the fimbriae or nonfimbri ated E. coli, type 1 fimbriated E. coli induced mast cell degranulatio n in vitro. The magnitude of mast cell degranulation was directly prop ortional to the number of adherent bacteria on the cell surface in the initial period of the interaction. Using a mouse model of bacterial p eritonitis, we demonstrated mast cell degranulation and histamine rele ase by type 1 fimbriated bacteria in vivo. Furthermore, beads coated w ith FimH but not with FimA, the major subunit of type 1 fimbriae, evok ed mast cell release of histamine in vivo in amounts comparable to tha t elicited by type 1 fimbriated E. coli. These studies reveal that mas t cells can be degranulated by interaction with type 1 fimbriated E. c oli and that FimH, the mannose-binding component of the fimbriae, is a potent mast cell stimulant.