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PIE cell line: Control vs. ETEC treated or Immunobiotic treated

ABSTRACT: We investigate the transcriptome response of porcine intestinal epitheliocyte cell line (PIE cells) to the challenge with heat-stable Enterotoxigenic Escherichia coli (ETEC) pathogen-associated molecular patterns (PAMPs) and, the changes induced by Lactobacillus jensenii TL2937 in that response. The transcriptome approach allowed us to obtain a global overview of the immune and immune related genes involved in response of PIE cells to heat-stable ETEC PAMPs. The most remarkable changes in PIE cells after heat-stable ETEC PAMPs challenge were observed in chemokines expressions, followed by cell adhesion molecules and, complement and coagulation cascades factors. We also confirmed that L. jensenii TL2937 differently modulates gene expression in ETEC PAMPs-challenged PIE cells. The microarray gene expression profiles clearly demonstrated that an anti-inflammatory effect was triggered by the immunobiotic strain in PIE cells. The main outcome from the study was the differential regulation of chemokines (CCL8, CXCL5, CXCL9, CXCL10 and CXCL11), complement factors (C1R, C1S, C3 and CFB) and, coagulation system proteins (Tissue factor) expression by L. jensenii TL2937. PIE cells treated with the negative control Lactobacillus plantarum TL2766 showed a transcriptomic response similar to ETEC PAMPs-challenged PIE cells.

ORGANISM(S): Sus scrofa

PROVIDER: GSE77095 | GEO | 2016/01/22

SECONDARY ACCESSION(S): PRJNA309423

REPOSITORIES: GEO

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Project description:We investigated the transcriptome response of porcine intestinal epitheliocyte cell line (PIE cells) to the challenge with the Toll-like receptor 3 (TLR3) agonist poly(I:C) and, the changes induced by immunobiotic Lactobacillus rhamnosus CRL1505 (Lr1505) or Lactobacillus plantarum CRL1505 (Lp1506) in that response. The transcriptome approach allowed us to obtain a global overview of the immune and immune related genes involved in response of PIE cells to the viral pathogen-associated molecular pattern poly(I:C). The most remarkable changes in PIE cells after Poly(:IC) challenge were observed in type I interferons and, interferon-induced genes, cytokines and chemokines expressions, followed by cell adhesion molecules and, prostaglandins. Previous work demonstrated in vitro and in vivo the capacity of both Lr1505 and Lp1506 to improve antiviral immunity. Here, we also confirmed that both immunobiotic lactobacilli differently modulates gene expression in poly(I:C)-challenged PIE cells. The microarray gene expression profiles demonstrated that Lr1505 and Lp1506 increased the expression of type I interferons as well as the antiviral factors MX1, MX2, OAS1, OASL, RNASE4 and RNASEL. In addition, lactobacilli were able to significantly improve the expression of cytokines (IL-1β, IL-6), chemokines (AMCF-II, CCL20, CCL28, CCL4, CXCL10, CXCL11) and, adhesion molecules (SEL-E, SEL-L, EPCAM, ICAM-1). Of interest, both Lr1505 and Lp1506 differentially modulated the expression of several genes related to prostaglandins including PTGS2, PTGIR, PTGES and, PTGFRN. The results show the ability of Lr1505 and Lp1506 to increase cellular factors involved in innate antiviral immunity that would explain their capacity to increase resistance to viral challenges observed in animal models. In addition, Lr1505 and Lp1506 may potentiate antiviral immunity by promoting the recruitment and activation of immune cells via the factors produced by the epithelial cells. The comprehensive analysis of gene expression in PIE cells by microarray allowed an important advance in the understanding of the mechanisms of action involved in the antiviral effect of immunobiotic lactobacilli.

Project description:Enterotoxigenic Escherichia coli (ETEC) strains that produce both heat-stable (ST) and heat-labile (LT) enterotoxins cause severe post-weaning diarrhea in piglets. However, the relative importance of the individual enterotoxins to the pathogenesis of ETEC infection is poorly understood. In this study, we investigated the effect on virulence of an F4+ ETEC strain when removing some or all of its enterotoxins. Several isogenic mutant strains were constructed that lack the expression of LT in combination with one or both types of ST enterotoxins (STa and/or STb). Host early immune responses induced by these mutant strains 4h after infection were compared to the wild type strain GIS26 Â (O149:F4ac+, Â LT+ Â STa+ Â STb+). At the same time, the immune response of this wild type ETEC strain was compared to the mock-infected control, demonstrating the expression of porcine inflammatory response genes. For these purposes, the small intestinal segment perfusion (SISP) technique and microarray analysis were used and results were validated by qRT-PCR. We also measured net fluid absorption of pig small intestinal mucosa 4h after infection with wild type ETEC, the mutant strains and PBS (mock-infected). These data indicate an important role for STb in inducing small intestinal secretion early after infection. The microarray analysis of the different mutant strains also revealed an important role for STb in ETEC-induced immune response by the significant differential regulation of immune mediators like matrix metalloproteinase 3, interleukin 1 and interleukin 17. We conclude that STb can play a prominent role in ETEC-induced secretion and early immune response. In three pigs, 6 different treatments were performed. These treatments consisted of 4 mutant enterotoxigenic Escherichia coli GIS26 strains, GIS26 wild type strain, or PBS control. Per pig, the small intestine was divided into 6 loops with an interloop in between to avoid cross-contamination. In conclusion, every pig received each of the 6 treatments ad random.

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PIE cell line: Control vs. ETEC treated or Immunobiotic treated

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