Proteomic Analysis of IPEC‐J2 Cells in Response to Coinfection by Porcine Transmissible Gastroenteritis Virus and Enterotoxigenic Escherichia coli K88

Abstract

Based on these data, the authors suspect that integrin α5 might enable TGEV to promote ETEC K88 adhesion. This study is the first to analyze piglet diarrhea caused by TGEV-ETEC K88 coinfection using high-throughput quantitative proteomics. The results advance the understanding of coinfection and its role in causing piglet diarrhea.

Understanding TGEV–ETEC Coinfection through the Lens of Proteomics: A Tale of Porcine Diarrhea

“…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.…”

“…This raises many questions concerning the pathogenesis of coinfections. In a recent issue of Proteomics Clinical Applications , Xia and colleagues unveiled that TGEV infection augments the attachment of ETEC to intestinal cells, thence altering host cell homeostasis and the production of inflammatory cytokines (Figure ).…”

“…In this regard, the IPEC‐J2 cell line is an appropriate model since they are morphologically differentiated cells derived from the small intestine of young piglets . Using these cells, Xia and colleagues investigated the dynamics of coinfection by TGEV and ETEC . The authors showed that TGEV is able to grow and persist in IPEC‐J2 cells.…”

“…Using these cells, Xia and colleagues investigated the dynamics of coinfection by TGEV and ETEC . The authors showed that TGEV is able to grow and persist in IPEC‐J2 cells. Importantly, the authors found that a preexisting TGEV infection augmented ETEC attachment to intestinal cells.…”

“…To gain important insight into how TGEV promotes ETEC attachment, Xia et al. undertook a comparative proteomics approach where they employed LC–MS/MS coupled to iTRAQ to study cells infected with TGEV, ETEC, or both . Relative to noninfected cells, TGEV infection modulated the expression of 77 proteins.…”