pORF5 plasmid protein of Chlamydia trachomatis induces MAPK-mediated pro-inflammatory cytokines via TLR2 activation in THP-1 cells

Hui Zhou, Qiu Lin Huang, Zhong Yu Li, Yi Mou Wu, Xiao Bing Xie, Kang Kang Ma, Wen Juan Cao, Zhou Zhou, Chun Xue Lu, Guang Ming Zhong

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Infection with Chlamydia trachomatis induces inflammatory pathologies in the urogenital tract that can lead to infertility and ectopic pregnancy. Pathogenesis of infection has been mostly attributed to excessive cytokine production. However, precise mechanisms on how C. trachomatis triggers this production, and which protein(s) stimulate inflammatory cytokines remains unknown. In the present study, the C. trachomatis pORF5 protein induced tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-8 (IL-8) in dose- and time-dependent manners in the THP-1 human monocyte cell line. We found that intracellular p38/mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK)/MAPK signaling pathways were required for the induction of TNF-α, IL-1β and IL-8. Blockade of toll-like receptor 2 (TLR2) signaling reduced induction levels of TNF-α, IL-8 and IL-1β. We concluded that the C. trachomatis pORF5 protein might contribute to the inflammatory processes associated with chlamydial infections.

Original languageEnglish (US)
Pages (from-to)460-466
Number of pages7
JournalScience China Life Sciences
Volume56
Issue number5
DOIs
StatePublished - May 7 2013

Keywords

  • Chlamydia trachomatis
  • TLR2
  • mitogen-activated protein kinase
  • pORF5 plasmid protein
  • proinflammatory cytokines

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Environmental Science(all)
  • Agricultural and Biological Sciences(all)

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