Role of cloned virulence factors (mannose-resistant haemagglutination, mannose-resistant adhesions) from uropathogenic Escherichia coli strains in the release of inflammatory mediators from neutrophils and mast cells.

Genetically cloned E. coli strains expressing cloned virulence factors were studied with regard to their capability to induce inflammatory mediator release from various target cells. Among the strains were E. coli strains with mannose-resistant haemagglutination (MRH+) and mannose-resistant adhesins, e.g. E. coli 536/21 pANN 801/4, E. coli 536/21 pANN 921 and E. coli 536/21 pANN 801-1. In comparison, E. coli 536/21, E. coli 536/21 pGB 30 int and E. coli K12, without and with mannose-sensitive haemagglutination (MSH +/-), and adhesins were studied. The properties of the various strains for human PMN with regard to adherence and phagocytosis, chemiluminescence, 5-lipoxygenase activation of arachidonic acid, leukotriene formation, granular enzyme release and release of histamine from rat mast cells were analysed. It is evident that the various biochemical processes of cell activation are dissociated events. The highest chemiluminescence response is obtained with strains expressing MSH+, P-MRH+ or S-MRH+; the presence of S-adhesins suppressed the response. Highest leukotriene formation is obtained with E. coli 536/21 pANN 801-4, while E. coli with MSH was inactive. The concomitant presence of haemolysin secretion enhanced mediator release significantly. Our data suggest a potent role for mannose-resistant haemagglutination (MRH), adhesins and haemolysin as virulence factors in inducing the release of inflammatory mediators.