Abstract
Enterotoxigenic Escherichia coli (ETEC) causes childhood diarrhea in developing countries. ETEC strains produce the heat-labile enterotoxin (LT) and/or heat-stable enterotoxins (ST) and encode a diverse set of colonization factors used for adherence to intestinal epithelial cells. We previously found that ETEC secretes a heat-stable protein we designated as ETEC Secreted Factor (ESF) that inhibits the extent of NF-κB activation normally induced by tumor necrosis factor alpha (TNF). Here we fractionated ETEC supernatants using fast protein liquid chromatography (FPLC) and determined that ETEC flagellin was necessary and sufficient to protect IκBα from degradation in response to TNF stimulation. These data suggest a potentially novel mechanism by which ETEC may evade the host innate immune response by down-regulating NF-κB-dependent host responses.
Highlights
Enterotoxigenic Escherichia coli (ETEC) causes travelers’ diarrhea and diarrheal disease in children living in developing countries [1,2]
We previously reported that pre-incubation of HCT-8 cells with ETEC H10407 supernatant prevented tumor necrosis factor alpha (TNF) stimulation from inducing IκBα degradation and nuclear factor-κB (NF-κB) activation [14]
We attributed prevented TNF stimulation from inducing IκBα degradation and NF-κB activation [14]. We attributed this result to a heat-stable protein we designated as ETEC Secreted Factor (ESF)
Summary
Enterotoxigenic Escherichia coli (ETEC) causes travelers’ diarrhea and diarrheal disease in children living in developing countries [1,2]. ETEC strains encode two main types of virulence factors—heat-labile and/or heat-stable toxins (LT and ST)—that cause watery diarrhea [3] and colonization factors (CFs) that mediate ETEC adherence to intestinal enterocytes [4]. Upon TNF stimulation or microbial infection, the IκB kinase (IKK) complex is activated and phosphorylates IκBα which is polyubiquitinated and degraded, resulting in nuclear translocation of NF-κB subunits [11]. We previously reported that pre-incubation of HCT-8 cells with ETEC H10407 supernatant prevented TNF stimulation from inducing IκBα degradation and NF-κB activation [14]. We attributed prevented TNF stimulation from inducing IκBα degradation and NF-κB activation [14]. We attributed this result to a heat-stable protein we designated as ETEC Secreted Factor (ESF).
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