Wang Gaochan, Geisbrecht Brian V, Rueter Christian, Hardwidge Philip R
Department of Diagnostic Medicine/Pathobiology, Kansas State University, Manhattan, KS 66506, USA.
Department of Biochemistry and Molecular Biophysics, Kansas State University, Manhattan, KS 66506, USA.
Pathogens. 2017 May 17;6(2):18. doi: 10.3390/pathogens6020018.
Enterotoxigenic (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.
产肠毒素大肠杆菌(ETEC)在发展中国家可导致儿童腹泻。ETEC菌株产生不耐热肠毒素(LT)和/或耐热肠毒素(ST),并编码多种用于黏附肠上皮细胞的定植因子。我们之前发现,ETEC分泌一种热稳定蛋白,我们将其命名为ETEC分泌因子(ESF),该因子可抑制肿瘤坏死因子α(TNF)正常诱导的核因子κB(NF-κB)激活程度。在这里,我们使用快速蛋白质液相色谱法(FPLC)对ETEC上清液进行分级分离,并确定ETEC鞭毛蛋白对于保护IκBα免受TNF刺激诱导的降解是必要且充分的。这些数据提示了一种潜在的新机制,通过该机制ETEC可能通过下调NF-κB依赖的宿主反应来逃避宿主固有免疫反应。