Increased arthritis severity in mice coinfected with Borrelia burgdorferi and Babesia microti

Manuel H Moro1, Ofelia L Zegarra-Moro, Johannes Bjornsson

  • 1Department of Immunology, Mayo Foundation, Rochester, Minnesota, MN, USA. moro.manuel@mayo.edu

Insights

Coinfection with Babesia microti and Borrelia burgdorferi can worsen arthritis in mice. This Lyme disease coinfection model showed increased severity linked to reduced IL-10 and IL-13 cytokine expression.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Pathology

Background:

  • Simultaneous Borrelia burgdorferi (Lyme disease agent) and Babesia microti infections are reported with increased disease severity.
  • Understanding coinfection dynamics is crucial for diagnosing and treating tick-borne illnesses.

Purpose of the Study:

  • To investigate if coinfection with Babesia microti exacerbates Borrelia burgdorferi-induced arthritis and carditis in a murine model.
  • To correlate observed disease severity with specific cytokine expression profiles.

Main Methods:

  • Murine models (C3H.HeJ and BALB/c mice) were infected with either B. burgdorferi alone or coinfected with B. microti and B. burgdorferi.
  • Mice were monitored for 15 and 30 days post-inoculation.
  • Arthritis and carditis severity were assessed via histopathology; cytokine levels (IFN-γ, IL-4, IL-10, IL-13) were measured in supernatants.

Main Results:

  • No significant differences in disease severity were observed in C3H.HeJ mice.
  • BALB/c mice coinfected with B. microti and B. burgdorferi exhibited significantly increased arthritis severity at day 30.
  • This heightened arthritis correlated with significantly reduced expression of interleukin-10 (IL-10) and interleukin-13 (IL-13).

Conclusions:

  • Coinfection with Babesia microti can worsen Borrelia burgdorferi-induced arthritis in susceptible mouse strains (BALB/c).
  • The exacerbation of arthritis in coinfected mice is associated with a suppressed immune response, indicated by reduced IL-10 and IL-13 levels.
  • These findings highlight the complex interplay between tick-borne pathogens and host immune responses.

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