Probiotics induce intestinal IgA secretion in weanling mice potentially through promoting intestinal APRIL expression and modulating the gut microbiota composition

Food Funct. 2024 May 7;15(9):4862-4873. doi: 10.1039/d4fo00962b.

Abstract

Intestinal infections are strongly associated with infant mortality, and intestinal immunoglobulin A (IgA) is important to protect infants from intestinal infections after weaning. This study aims to screen probiotics that can promote the production of intestinal IgA after weaning and further explore their potential mechanisms of action. In this study, probiotics promoting intestinal IgA production were screened in weanling mouse models. The results showed that oral administration of Bifidobacterium bifidum (B. bifidum) FL228.1 and Bifidobacterium bifidum (B. bifidum) FL276.1 significantly enhanced IgA levels in the small intestine and upregulated the expression of a proliferation-inducing ligand (APRIL) and its upstream regulatory factor toll-like receptor 4 (TLR4). Furthermore, B. bifidum FL228.1 upregulated the relative abundance of Lactobacillus, while B. bifidum FL276.1 increased the relative abundance of Marvinbryantia and decreased Mucispirillum, further elevating intestinal IgA levels. In summary, B. bifidum FL228.1 and B. bifidum FL276.1 can induce IgA production in the intestinal tract of weanling mice by promoting intestinal APRIL expression and mediating changes in the gut microbiota, thus playing a significant role in enhancing local intestinal immunity in infants.

MeSH terms

  • Animals
  • Bifidobacterium bifidum* / physiology
  • Female
  • Gastrointestinal Microbiome*
  • Immunoglobulin A*
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Intestines / immunology
  • Intestines / microbiology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Probiotics* / administration & dosage
  • Probiotics* / pharmacology
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor Ligand Superfamily Member 13* / genetics
  • Tumor Necrosis Factor Ligand Superfamily Member 13* / metabolism
  • Weaning

Substances

  • Immunoglobulin A
  • Tumor Necrosis Factor Ligand Superfamily Member 13
  • Toll-Like Receptor 4