4.2 Article

Relevant fecal microbes isolated from mice with food allergy elicited intestinal cytokine/chemokine network and T-cell immune responses

Journal

BIOSCIENCE OF MICROBIOTA FOOD AND HEALTH
Volume 39, Issue 4, Pages 234-242

Publisher

BMFH PRESS
DOI: 10.12938/bmfh.2020-014

Keywords

cytokine/chemokine network; dysbiosis; fecal microbiota; food allergy; T-cell response

Funding

  1. Ministry of Science and Technology, Taiwan [MOST-107-2320-B-019-003, MOST-108-2320-B-019-006]

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The objective of this study was to identify the relevant fecal microbes from mice with food allergy and investigate the impact of these microbes on intestinal epithelial cells and allergen-specific T-cell responses. A murine model of ovalbumin (OVA)-induced food allergy was employed. The profile of fecal microbiota was evaluated by the traditional plating method and next-generation sequencing (NGS) of the 16S ribosomal RNA gene. The density of fecal bacteria growth on RCM, TSA and LB plates was elevated in mice with food allergy, whereas the diversity of fecal bacteria was decreased. Additionally, the relative abundances of Prevotellaceae and Prevotella were increased. The isolated fecal strains, mostly belonging to Enterococcus, Streptococcus and Vagococcus, significantly reduced the viability of intestinal Caco-2 cells but increased the production of interleukin (IL)-8, C-C motif chemokine ligand (CCL)-2, CCL-5, CCL-20 and C-X-C motif chemokine ligand (CXCL)-1. Moreover, cell expansion and secretion of IL-2, interferon (IFN)-gamma, IL-4 and IL-17 by mesenteric lymph node (MLN) cells were augmented, whereas the production of IL-10 and transforming growth factor (TGF)-beta was diminished. Although individual fecal strains had varying degrees of impact on Caco-2 cells and MLN cells, these results precisely indicate a different profile of fecal microbiota between normal mice and allergic mice. Most important, the relevant fecal microbes involved in allergen-induced dysbiosis have the potential to induce intestinal cytokine/ chemokine network and T-cell immune responses.

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