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The inflammatory cytokine response to Chlamydia trachomatis infection is endotoxin mediated

R R Ingalls1, P A Rice, N Qureshi

  • 1Maxwell Finland Laboratory for Infectious Diseases, Boston City Hospital, Massachusetts, USA.

Infection and Immunity
|August 1, 1995
PubMed

Insights

Chlamydia trachomatis lipopolysaccharide (LPS) weakly induces inflammatory responses, explaining its often asymptomatic infections. This suggests LPS is the primary mediator of chlamydial immune responses.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Chlamydia trachomatis is a major cause of sexually transmitted diseases.
  • Despite being gram-negative, chlamydial infections are not typically viewed as endotoxin-mediated.
  • The acute immune response to C. trachomatis, particularly the role of its lipopolysaccharide (LPS), requires molecular characterization.

Purpose of the Study:

  • To molecularly characterize the acute immune response to C. trachomatis, focusing on the role of its lipopolysaccharide (LPS).
  • To analyze the structure and biological activity of C. trachomatis LPS.
  • To compare the endotoxin activities of C. trachomatis with other bacterial pathogens.

Main Methods:

  • Lipopolysaccharide (LPS) was extracted from C. trachomatis elementary bodies (EB).
  • Methylated lipid A was analyzed using high-pressure liquid chromatography and mass spectrometry.
  • Endotoxin activities were assessed by measuring tumor necrosis factor alpha release from whole blood and nuclear factor kappa B translocation in a CD14-transfected cell line, comparing C. trachomatis with Salmonella minnesota and Neisseria gonorrhoeae.

Main Results:

  • The majority of C. trachomatis lipid A was found to be pentaacylated.
  • Both purified C. trachomatis LPS and whole EB induced tumor necrosis factor alpha release and nuclear factor kappa B translocation.
  • C. trachomatis LPS and EB were approximately 100-fold less potent than Salmonella and Neisseria gonorrhoeae in inducing these inflammatory responses.
  • Specific LPS antagonists inhibited the TNF-alpha-inducing activity of C. trachomatis EB.

Conclusions:

  • C. trachomatis is a weak inducer of inflammatory cytokine responses, correlating with its often asymptomatic clinical presentation.
  • The lipopolysaccharide (LPS) of C. trachomatis appears to be the primary mediator of the inflammatory cytokine response during chlamydia infection.
  • The role of other C. trachomatis surface protein antigens in eliciting a proinflammatory cytokine response is likely minor.

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