Abstract

Bacterial exopolysaccharides (EPSs) are known to modulate immunity. To date, a plethora of studies have reported the effect of EPSs on intestinal cells; however few works have revealed a complete picture of the signalling events in intestinal epithelial cells induced by bacterial EPSs. Here, using transcriptomics, we comprehensively mapped the biological processes in porcine intestinal epithelial cells challenged with EPS derived from Lactobacillus reuteri alone, enterotoxigenic Escherichia coli (ETEC) or ETEC after pretreatment with EPS. The Gene Ontology analysis of differentially expressed genes (DEGs) showed that ETEC is able to evoke biological processes specifically involved in cell junction reorganization, extracellular matrix degradation, and activation of the innate immune response through the activation of pattern recognition receptors, such as TLRs and CTRs. A total of 495 DEGs were induced in ETEC-challenged cells. On the other hand, EPS pretreatment was able to attenuate overexpression of the genes induced by ETEC infection. The most relevant finding of this study is that EPS has a suppressive effect on the inflammatory response evoked by ETEC infection. On the basis of high-throughput RNA-seq, this report is the first to describe the effects of EPSs derived from L. reuteri used as a pretreatment of global gene expression in porcine epithelial cells.

Highlights

  • Bacterial exopolysaccharides (EPSs) are extracellular polysaccharides that play pivotal roles in the protection of bacteria and adhesion to host cells

  • E. coli induced the regulation of calmodulin-dependent protein kinase II (CAMKII) (CAMK2G); the upregulation was attenuated by EPS pretreatment (Figure 8)

  • EPS pretreatment can reduce the overexpression of PRKAR1A and CAMK2G, which are activated in E. coli infection

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Summary

Introduction

Bacterial exopolysaccharides (EPSs) are extracellular polysaccharides that play pivotal roles in the protection of bacteria and adhesion to host cells. Enterotoxigenic Escherichia coli (ETEC) is one of the most common causes of post-weaning diarrhea in pigs [9, 10]. ETEC interacts with epithelial cells, colonizes the small intestine and secretes thermostable (ST) or Tkáčiková et al Vet Res (2020) 51:49 thermolabile (LT) enterotoxins, inducing acute intestinal diarrhea and inflammation [11]. ETEC infection is responsible for economic losses in the pig industry mainly due to high mortality, morbidity, growth retardation and treatment costs [12]. It is necessary to protect piglets against ETEC infection by modulating their gut immunity with prebiotics, probiotics or the products of beneficial bacteria such as EPSs

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