TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo

PLoS One. 2017 Oct 9;12(10):e0186179. doi: 10.1371/journal.pone.0186179. eCollection 2017.

Abstract

Toll-like receptors (TLRs) 2 and 4 play critical roles in intestinal inflammation caused by Fusobacterium nucleatum (F. nucleatum) infection, but the role of TLR2/TLR4 in regulation of proinflammatory cytokines remains unknown. In this study, through microarray analysis and qRT-PCR, we showed that TLR2/TLR4 are involved in the F. nucleatum-induced inflammatory signaling pathway in Caco-2 cells, C57BL/6 mice and human clinical specimens. In TLR2-/- and TLR4-/- mice, F. nucleatum infection resulted in increased colonization of the bacteria and production of the proinflammatory cytokines IL-8, IL-1β and TNF-α. In addition, the ratio of Foxp3+ CD4+ T cells in the total CD4+ T cells in TLR2-/- and TLR4-/- mice was less than that in wild-type mice, and the ratio in hybrid mice was more than that in knockout mice, which suggested that TLR2/TLR4 mediated the number of Tregs. Furthermore, it was observed that inflammatory cytokine levels were reduced in TLR2-/- mice after Treg transfer. Thus, these data indicate that TLR2/TLR4 regulate F. nucleatum-induced inflammatory cytokines through Tregs in vivo.

MeSH terms

  • Adult
  • Animals
  • Caco-2 Cells
  • Female
  • Fusobacterium Infections / immunology*
  • Fusobacterium Infections / microbiology
  • Fusobacterium Infections / pathology
  • Fusobacterium nucleatum / immunology
  • Fusobacterium nucleatum / pathogenicity
  • Humans
  • Inflammation / genetics
  • Inflammation / immunology*
  • Inflammation / microbiology
  • Intestines / microbiology
  • Intestines / pathology
  • Male
  • Mice
  • Mice, Knockout
  • Microarray Analysis
  • Middle Aged
  • Signal Transduction
  • T-Lymphocytes, Regulatory / immunology
  • Toll-Like Receptor 2 / genetics*
  • Toll-Like Receptor 2 / immunology
  • Toll-Like Receptor 4 / genetics*
  • Toll-Like Receptor 4 / immunology

Substances

  • Tlr2 protein, mouse
  • Tlr4 protein, mouse
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4

Grants and funding

This work was supported by Grant Nos. 81501796 (for Q.L.) from National Natural Science Foundation of China (NSFC,), and the project of medical science and technology for training youth scholars of PLA (14QNP054) (for B.T.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.