Murine Lyme disease: no evidence for active immune down-regulation in resolving or subclinical infection

R R Montgomery1, X M Wang, S E Malawista

  • 1Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8031, USA. ruth.montgomery@yale.edu

Insights

Macrophages combat Borrelia burgdorferi, but survival can cause Lyme disease complications. This study found no evidence of immune system down-regulation in infected mouse hearts, suggesting inflammation is not suppressed.

Area of Science:

  • Immunology
  • Microbiology
  • Pathology

Background:

  • Macrophages are crucial in fighting Borrelia burgdorferi (Lyme disease agent).
  • Spirochete survival in vivo may involve immune system suppression.
  • Understanding macrophage activation in Lyme disease is vital for treatment.

Purpose of the Study:

  • To evaluate macrophage activation in active Lyme disease sites.
  • To assess cytokine expression in murine macrophages during Borrelia burgdorferi infection.
  • To determine if immune down-regulation occurs in infected host tissues.

Main Methods:

  • Double-label immunofluorescent staining in situ for cytokine detection.
  • Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) for mRNA analysis.
  • Analysis of macrophages from infected murine hearts and peritoneal cavities.

Main Results:

  • Infiltrating macrophages in infected hearts produced interleukin-1 (IL-1).
  • Increased mRNA levels for pro-inflammatory cytokines (IL-1, TNF-α, IL-12) were observed in infected hearts.
  • No increase in anti-inflammatory cytokines (IL-10, TGF-β) or cytokine changes in the peritoneal cavity were detected.

Conclusions:

  • Macrophage activation with pro-inflammatory cytokine production occurs in infected heart tissue during Lyme disease.
  • There is no evidence of immune down-regulation in the tested regions.
  • Inflammatory activity is not suppressed in active Lyme disease sites studied.

Related Concept Videos