Effects of adhesins from mannose-resistant Escherichia coli on mediator release from human lymphocytes, monocytes, and basophils and from polymorphonuclear granulocytes

Abstract

We investigated the role of Escherichia coli expressing mannose-resistant hemagglutination and adhesins with regard to the induction of leukotrienes from a suspension of human lymphocytes, monocytes, and basophils (LMBs) compared with human polymorphonuclear granulocytes (PMNs). Genetically cloned E. coli strains expressing various types of mannose-resistant hemagglutination (MRH+) were phagocytosed to a higher degree by monocytes than the nonadherent E. coli strain. The various strains differed in their capacity to induce a chemiluminescence response, which showed the same pattern for LMBs and PMNs. Stimulation of LMBs with bacteria alone, unlike granulocytes, did not activate the cells for the release of leukotrienes. However, preincubation of LMBs with bacteria decreased subsequent leukotriene formation when the cells were stimulated with calcium ionophore. The inhibitory effect was dependent on the concentration of bacteria used for preincubation as well as on the preincubation temperature. The various bacterial strains differed in inhibitory potency for mediator release. Preincubation of LMBs with zymosan, opsonized zymosan, the bacterial peptide FMLP, and peptidoglycan had no inhibitory effect or even increased subsequent leukotriene formation. Opsonized bacteria were far less inhibitory than nonopsonized bacteria. In contrast to human LMBs, preincubation of human PMNs with mannose-resistant bacteria led to increased leukotriene B4 generation and reduced w-oxidation of leukotriene B4. Our data suggest that phagocytes (neutrophils, monocytes) respond in a different way for leukotriene formation after interaction with mannose-resistant E. coli.

Septicemia-inducing Escherichia coli O115:K"V165"F165(1) resists killing by porcine polymorphonuclear leukocytes in vitro: role of F165(1) fimbriae and K"V165" O-antigen capsule

“…Bacteria expressing these fimbriae are associated with newborn meningitis and urinary tract infection, respectively, in humans. However, a genetically cloned strain expressing the S adhesin together with S fimbriae adheres to PMNLs but is less phagocytosed than the clone expressing S adhesin but not S fimbriae and does not induce an oxidative response (41). Thus, it appears that the presence of certain fimbriae such as S, irrespective of the presence of the fimbrial adhesin, may be involved in uptake and subsequent oxidative response of PMNLs.…”

Nonlethal adherence to human neutrophils mediated by Dr antigen-specific adhesins of Escherichia coli

“…Adherence of E. coli to PMNs and other effector cells mediated by type 1 fimbriae and S fimbriae is known to result in a variety of responses from the host cells, including stimulation of the respiratory burst, release of granular contents and other mediators, and increased arachidonate metabolism (17,52). These effects may result in host injury and promote the inflammatory response, thereby contributing to disease pathogenesis.…”

“…The nonfimbrial adhesin NFA-1 also mediates adherence to and stimulation of PMNs (13). In contrast, P fimbriae do not mediate adherence to PMNs (48,52), probably because PMNs lack membrane glycolipid receptors for P fimbriae (6,28,48).…”