Interaction of Escherichia coli with different fimbriae and polymorphonuclear leukocytes.
The effects of Escherichia coli strains with various fimbriae on bacteria-polymorphonuclear leukocyte (PMN) interactions were studied. Strains of E. coli were cultivated at 37 degrees C to express and at 18 degrees C to suppress the formation of fimbriae. The presence of fimbriae was confirmed by electron microscopic studies and hemagglutination and salt aggregation tests. Fimbriated E. coli strains were more readily PMN associated than the nonfimbriated strains in the absence of opsonins, confirming the results of previous studies. However, the PMN chemiluminescence (CL) induced by the various strains in the absence of serum opsonins depended on the type of fimbriae they expressed. Strains with type 1 fimbriae expressing mannose-sensitive hemagglutination induced 5 to 15 times more CL than the same strains grown at 18 degrees C, i.e., not expressing this type of fimbriae. For strains showing mannose-resistant hemagglutination, the differences between fimbriated and nonfimbriated variants of the same strains grown at 37 and 18 degrees C, respectively, were less pronounced. Analysis of enterotoxigenic strains expressing colonization factor antigen I (CFA/I) fimbriae showed that these induced only 25 to 33% of the CL induced by the same E. coli strains not expressing CFA/I, whereas enterotoxigenic strains expressing CFA/II fimbriae induced 100 to 200% of the CL induced by the nonfimbriated variants. Although less CL was induced by bacteria with CFA/I fimbriae than by nonfimbriated variants, this situation was reversed when the microorganisms were opsonized. Thus, CFA/I fimbriae, while enhancing adhesion to cells, induce less activation of PMN-killing mechanisms in a serum-free environment. These findings may be relevant for the virulence in certain body sites, since CFA/I fimbriae, while facilitating adhesiveness, may protect the bacteria from PMN killing. Our findings indicate that PMN interactions with fimbriated E. coli in the host defense may be complex. Certain fimbriae may indeed be advantageous to the bacteria, enabling them to interact with PMNs without activating the bactericidal oxidative metabolism.
D000268:Adhesiveness; D000942:Antigens, Bacterial / Q000276:immunology; D004926:Escherichia coli / Q000276:immunology* / Q000648:ultrastructure; D036781:Fimbriae Proteins; D010861:Fimbriae, Bacterial / Q000276:immunology*; D006801:Humans; D008163:Luminescent Measurements; D009504:Neutrophils / Q000276:immunology*; D009895:Opsonin Proteins; D010587:Phagocytosis
D000942:Antigens, Bacterial; D009895:Opsonin Proteins; C022924:colonization factor antigens; D036781:Fimbriae Proteins