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

摘要

Scope Piglet diarrhea causes large economic losses to the swine industry. Epidemiological investigations show that piglet diarrhea is often caused by mixed infections, but the mechanisms by which multiple microorganisms cause disease are unclear. Experimental design Because transmissible gastroenteritis virus (TGEV) and enterotoxigenic Escherichia coli K88 (ETEC K88) are important contributors to piglet diarrhea, coinfection experiments are conducted using porcine intestinal columnar epithelial cells (IPEC‐J2) as a model system. In order to evaluate piglet diarrhea caused TGEV and ETEC K88, the authors examin the effects of coinfection in IPEC‐J2 cells. In TGEV pre‐infected IPEC‐J2 cells, ETEC K88 adhesion is enhanced over uninfected cells. ETEC K88 is also found to inhibit the proliferation of TGEV. Additionally, cytokine levels (IL‐1β, IL‐6, IL‐8, and TNF‐α) in coinfected cells are lower than cells infected by TGEV alone, and higher than cells infected by ETEC K88 alone. LCMS/MS coupled to isobaric tags for relative and absolute quantification (iTRAQ) is used to profile expressed proteins in IPEC‐J2 cells infected by TGEV alone, ETEC K88 alone, and by both agents together. Results 77, 89, and 136 differentially expressed proteins are identified in TGEV infected, ETEC K88 infected, and coinfected cells, respectively. Conclusion and clinical relevance 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.