Arango Duque Guillermo, Acevedo Ospina Hamlet Adolfo
INRS-Institut Armand-Frappier and Centre for Host-Parasite Interactions, Laval, QC, Canada.
Proteomics Clin Appl. 2018 May;12(3):e1700143. doi: 10.1002/prca.201700143. Epub 2018 Jan 31.
Porcine diarrhea and gastroenteritis are major causes of piglet mortality that result in devastating economic losses to the industry. A plethora of pathogens can cause these diseases, with the transmissible gastroenteritis virus (TGEV) and enterotoxigenic Escherichia coli K88 (ETEC) being two of the most salient. In the December 2017 issue of Proteomics Clinical Aplications, Xia and colleagues used comparative proteomics to shed light on how these microbes interact to cause severe disease . The authors discovered that TGEV induces an epithelial-mesenchymal transition-like phenotype that augments cell adhesion proteins mediating the attachment of ETEC to intestinal epithelial cells. Moreover, coinfection was found to modulate several host proteins that could bolster pathogen persistence. Importantly, the authors observed that ETEC suppresses the production of inflammatory cytokines induced by TGEV, which may in turn promote the long-term survival of both microbes.
猪腹泻和肠胃炎是导致仔猪死亡的主要原因,给养猪业造成了巨大的经济损失。大量病原体可引发这些疾病,其中传染性肠胃炎病毒(TGEV)和产肠毒素大肠杆菌K88(ETEC)是最突出的两种。在2017年12月的《蛋白质组学临床应用》杂志上,夏及其同事运用比较蛋白质组学来阐明这些微生物如何相互作用导致严重疾病。作者发现,TGEV诱导出一种上皮-间质转化样表型,增强了介导ETEC附着于肠道上皮细胞的细胞粘附蛋白。此外,发现共感染会调节几种宿主蛋白,这些蛋白可能会增强病原体的持久性。重要的是,作者观察到ETEC抑制了TGEV诱导的炎性细胞因子的产生,这反过来可能会促进两种微生物的长期存活。