Expression of TLR 2, TLR 4 and iNOS in cervical monocytes of Chlamydia trachomatis-infected women and their role in host immune response

Am J Reprod Immunol. 2011 Dec;66(6):534-43. doi: 10.1111/j.1600-0897.2011.01064.x. Epub 2011 Aug 24.

Abstract

Problem: To study the innate immune response -TLR2 TLR 4 and iNOS expression in female genital Chlamydia trachomatis infection.

Method: TLR 2, TLR 4, and iNOS expression was evaluated by real-time PCR in C. trachomatis-infected asymptomatic, mucopurulent cervicitis (MPC), and fertility disorders (FD) women. Expression of TLR signaling pathway genes was checked in vivo in C. trachomatis-infected cervical monocytes. Further, inos gene expression and nitric oxide release was assessed in vitro in THP-1 cell line upon chlamydial infection.

Results: TLR2, TLR4, and iNOS expression was significantly (P < 0.05) higher in C. trachomatis-positive women with FD, MPC, and asymptomatic women, respectively, than in control. Chlamydial infection significantly upregulates CD86, TLR4, MyD88, IRAK2, nF-κB, IL-1,β and IL-12 genes. Expression of iNOS gene was found to be significantly (P < 0.05) high 12 hrs post-infection.

Conclusions: Chlamydia trachomatis stimulates innate immune cells by activation of TLR2/TLR 4. Overall data indicate that recognition by TLR4 helps in initiation of immune response while recognition by TLR2 leads to secretion of inflammatory cytokines while iNOS-induced nitric oxide production helps in clearing Chlamydia. These results are first to provide initial insights into how innate immune response operates in human cervical monocytes upon chlamydial infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Line
  • Cervix Uteri / immunology*
  • Cervix Uteri / microbiology
  • Chlamydia Infections / immunology
  • Chlamydia Infections / microbiology
  • Chlamydia trachomatis / pathogenicity*
  • Female
  • Genital Diseases, Female / immunology
  • Genital Diseases, Female / microbiology
  • HeLa Cells
  • Humans
  • Immunity, Innate
  • Monocytes / immunology
  • Monocytes / metabolism*
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism*
  • Toll-Like Receptor 2 / genetics
  • Toll-Like Receptor 2 / metabolism*
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism*
  • Up-Regulation

Substances

  • Toll-Like Receptor 2
  • Toll-Like Receptor 4
  • NOS2 protein, human
  • Nitric Oxide Synthase Type II