Oligosaccharides Modulate Rotavirus-Associated Dysbiosis and TLR Gene Expression in Neonatal Rats

Cells. 2019 Aug 11;8(8):876. doi: 10.3390/cells8080876.

Abstract

Colonization of the gut in early life can be altered through multiple environmental factors. The present study aimed to investigate the effects of 2'-fucosyllactose (2'-FL), a mixture of short-chain galactooligosaccharides/long-chain fructooligosaccharides (scGOS/lcFOS) 9:1 and their combination (scGOS/lcFOS/2'-FL) on dysbiosis induced during rotavirus (RV) diarrhea in neonatal rats, elucidating crosstalk between bacteria and the immune system. The dietary interventions were administered daily by oral gavage at days 2-8 of life in neonatal Lewis rats. On day 5, RV SA11 was intragastrically delivered to induce infection and diarrhea assessment, microbiota composition, and gene expression of Toll-like receptors (TLRs) in the small intestine were studied. All dietary interventions showed reduction in clinical variables of RV-induced diarrhea. RV infection increased TLR2 expression, whereas 2'-FL boosted TLR5 and TLR7 expressions and scGOS/lcFOS increased that of TLR9. RV-infected rats displayed an intestinal dysbiosis that was effectively prevented by the dietary interventions, and consequently, their microbiota was more similar to microbiota of the noninfected groups. The preventive effect of 2'-FL, scGOS/lcFOS, and their combination on dysbiosis associated to RV diarrhea in rats could be due to changes in the crosstalk between gut microbiota and the innate immune system.

Keywords: HMOs; TLR; microbiota; rotavirus; scGOS/lcFOS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Diarrhea / drug therapy
  • Diarrhea / microbiology
  • Dysbiosis / chemically induced
  • Dysbiosis / drug therapy*
  • Dysbiosis / microbiology*
  • Female
  • Gastrointestinal Microbiome / drug effects*
  • Intestine, Small / microbiology*
  • Oligosaccharides / pharmacology*
  • Rats
  • Rats, Inbred Lew
  • Rotavirus
  • Rotavirus Infections / drug therapy
  • Rotavirus Infections / microbiology
  • Toll-Like Receptors / metabolism*

Substances

  • Oligosaccharides
  • Toll-Like Receptors