Analysis of the basal colonic innate immune response of pigs divergent in feed efficiency and following an ex vivo lipopolysaccharide challenge

Physiol Genomics. 2019 Sep 1;51(9):443-448. doi: 10.1152/physiolgenomics.00013.2019. Epub 2019 Jul 19.

Abstract

While feed efficiency is influenced by multiple physiological processes, it is not known how efficient and inefficient pigs differ in relation to their basal immune response, and particularly their innate immune response to a microbial challenge. Hence, the objective was to examine the expression of genes encoding innate immune response markers in basal colonic tissue and colonic tissue following an ex vivo lipopolysaccharide (LPS) challenge from pigs divergent in residual feed intake (RFI). Pigs that differed in RFI were selected from two different farms of origin. Colonic tissue was harvested from high RFI (HRFI) and low (LRFI) pigs, and two experimental conditions were explored: the first was basal unchallenged tissue and the second was colonic tissue following an ex vivo LPS challenge. RNA was extracted and tested on a Nanostring panel of 72 genes coding for barrier defense proteins, transmembrane receptors, kinases, transcription regulators, cytokines, and cytokine regulators. In the basal unchallenged tissue, the LRFI pigs had increased expression of AOAH, AP1, and TRAM and the cytokines TNF, IL10, and CXCL8, compared with the HRFI pigs (P < 0.05), with a significant effect of farm of origin on 31 genes (P < 0.05). In the LPS-challenged tissues, the LRFI group had higher expression of TLR1, TLR7, TLR8, GPR43/FFAR2, JAK2, and NFAM1 compared with the HRFI group (P < 0.05). In conclusion, these data suggest that LRFI pigs have an upregulated basal colonic inflammatory state and a heightened response to an LPS challenge compared with the inefficient HRFI pigs. This immune profile potentially enhances their capacity to respond to an infectious challenge.

Keywords: feed efficiency; lipopolysaccharide; pig; residual feed intake; transcriptome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animal Feed*
  • Animals
  • Colon / drug effects
  • Colon / immunology*
  • Cytokines / genetics
  • Eating / immunology*
  • Fasting
  • Gene Expression Regulation / drug effects
  • Immunity, Innate / drug effects
  • Immunity, Innate / genetics*
  • Janus Kinase 2 / genetics
  • Lipopolysaccharides / pharmacology*
  • Receptors, G-Protein-Coupled / genetics
  • Swine
  • Toll-Like Receptors / genetics
  • Transcriptome / drug effects

Substances

  • Cytokines
  • Lipopolysaccharides
  • Receptors, G-Protein-Coupled
  • Toll-Like Receptors
  • Janus Kinase 2