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1 Department of Medicine, Section of Digestive Diseases and Nutrition, University of Illinois at Chicago, Chicago, IL, USA
2 Department of Medicine, Section of Digestive Diseases and Nutrition, University of Illinois at Chicago, Chicago, IL, USA; Jesse Brown VA Medical Center, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: gahecht{at}uic.edu.
EPEC virulence requires a type III secretion system (TTSS) to deliver effector molecules into host cells. Although the TTSS is crucial to EPEC pathogenesis, its function in EPEC-induced inflammation is not known. The aim of this study was to investigate the role of the TTSS in EPEC-induced inflammation. HT-29 intestinal epithelial cells were infected with wild-type (WT) EPEC or select mutant strains or exposed to corresponding filter-sterilized supernatants (SN) and interleukin-8 (IL-8) secretion was determined by ELISA. EPEC SN stimulated significantly greater IL-8 production than EPEC organisms. Flagellin, as well as a TTSS-independent >50kDa non-flagellin protein, was found to significantly contribute to this response. Dose-response studies showed that increasing concentrations of WT SN proportionally increased IL-8, while increasing multiplicity of infection of EPEC inversely correlated with IL-8 secretion suggesting that EPEC dampens this host response. Infection with 
escN (non-functional TTSS) markedly increased IL-8 compared to WT indicating that a functional TTSS is required for this anti-inflammatory property; complementation of escN restored the attenuated response. Mutation of espB also enhanced the IL-8 response and complementation returned IL-8 to near WT levels suggesting involvement of this effector. The anti-inflammatory effect extends to both bacterial and host-derived pro-inflammatory stimuli as prior infection with EPEC suppressed the IL-8 response to TNF-
, IL-1
and EHEC flagellin. These findings indicate that EPEC-induced inflammation is a balance between pro- and anti-inflammatory proteins; extracellular factors, including flagellin and an unidentified TTSS-independent, >50kDa protein, trigger inflammation while intracellular TTSS-dependent factors including EspB attenuate this response.
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