Induction and suppression of cytokine release (tumour necrosis factor-alpha; interleukin-6, interleukin-1 beta) by Escherichia coli pathogenicity factors (adhesions, alpha-haemolysin).

Escherichia coli bacteria expressing mannose-resistant fimbriae/haemagglutination induced the production of substantial amounts of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) from a peripheral human lymphocyte, monocyte, basophil (LMB) cell suspension. In this regard, E. coli bacteria with S-mannose-resistant fimbriae/haemagglutination were the most potent inducers of IL-6 and TNF-alpha secretion, followed by the E. coli strain with P-mannose-resistant fimbriae/haemagglutination. The E. coli alpha-haemolysin did not stimulate cytokine release from human LMB. In fact, this toxin, at non-toxic concentrations, depressed the spontaneous as well as the E. coli-induced production of TNF-alpha, IL-6, IL-1 beta. Our results indicate that two mechanisms may contribute to the severity of E. coli infection: (a) stimulation of cytokine release by type-specific fimbriae/haemagglutination properties and (b) depression of immune response by the E. coli alpha-haemolysin.