[Intestinal dysbacteriosis promotes intestinal intraepithelial T lymphocyte activation and proinflammatory cytokine secretion in mice]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Aug;32(8):1031-5.
[Article in Chinese]

Abstract

Objective To study the effect of intestinal dysbacteriosis on mouse intestinal intraepithelial T lymphocytes (iIELs). Methods The intestinal dysbacteriosis was induced in mice by oral administration of ceftriaxone sodium. The iIELs were digested with ethylene diaminetetraacetic acid (EDTA) and DL-dithiothreitol (DTT). The phenotype of iIELs and the proportions of subsets of T cells were detected by flow cytometry; the concentrations of cytokines (IL-2, IL-6, IFN-γ) in the intestine were examined by ELISA; the intestinal bacteria were analyzed with selective medium and PCR. Results Compared with the control group, intestinal commensal bacteria in mice were significantly reduced after the administration of ceftriaxone sodium, but fungi and yeasts increased. The proportions of T cell subgroups in ilELs changed, in which the proportion of TCR γδ(+)T cells significantly increased, and the activated CD3(+)T, CD8(+)T and TCR γδ(+)T cells increased. The concentrations of IL-2, IL-6 and IFN-γ were significantly raised in the intestine. Conclusion The dysbacteriosis results in the decrease of commensal bacteria, the increase of the fungus, the damage of microbial barrier, the more activated T cells in ilELs and the promotion of proinflammatory cytokine secretion in the gut. This is probably one of the reasons for inflammatory bowel disease caused by dysbacteriosis.

MeSH terms

  • Animals
  • Antigens, CD / immunology
  • Antigens, CD / metabolism
  • Antigens, Differentiation, T-Lymphocyte / immunology
  • Antigens, Differentiation, T-Lymphocyte / metabolism
  • Bacteria / classification
  • Bacteria / genetics
  • Ceftriaxone
  • Cytokines / immunology*
  • Cytokines / metabolism
  • Dysbiosis / chemically induced
  • Dysbiosis / immunology*
  • Dysbiosis / metabolism
  • Flow Cytometry
  • Inflammation Mediators / immunology*
  • Inflammation Mediators / metabolism
  • Interferon-gamma / immunology
  • Interferon-gamma / metabolism
  • Interleukin-2 / immunology
  • Interleukin-2 / metabolism
  • Interleukin-6 / immunology
  • Interleukin-6 / metabolism
  • Intestinal Diseases / chemically induced
  • Intestinal Diseases / immunology*
  • Intestinal Diseases / metabolism
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Intestines / immunology
  • Intestines / microbiology
  • Lectins, C-Type / immunology
  • Lectins, C-Type / metabolism
  • Lymphocyte Activation / immunology
  • Male
  • Mice, Inbred BALB C
  • Polymerase Chain Reaction
  • RNA, Ribosomal, 16S / genetics
  • Receptors, Antigen, T-Cell, gamma-delta / immunology
  • Receptors, Antigen, T-Cell, gamma-delta / metabolism
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism

Substances

  • Antigens, CD
  • Antigens, Differentiation, T-Lymphocyte
  • CD69 antigen
  • Cytokines
  • Inflammation Mediators
  • Interleukin-2
  • Interleukin-6
  • Lectins, C-Type
  • RNA, Ribosomal, 16S
  • Receptors, Antigen, T-Cell, gamma-delta
  • Ceftriaxone
  • Interferon-gamma