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Mammalian antimicrobial peptide influences control of cutaneous Leishmania infection

Manjusha M Kulkarni1, Joseph Barbi, W Robert McMaster

  • 1Center for Microbial Interface Biology, The Ohio State University Medical Center, Columbus, OH, USA.

Cellular Microbiology
|April 20, 2011
PubMed

Insights

Cathelicidin-type antimicrobial peptides (CAMP) are crucial for controlling Leishmania parasite infections by modulating host immunity and preventing parasite spread. Lack of CAMP exacerbates lesions and promotes parasite dissemination, highlighting CAMP

Area of Science:

  • Immunology
  • Parasitology
  • Antimicrobial Peptides

Background:

  • Cathelicidin-type antimicrobial peptides (CAMP) are key innate immune mediators.
  • CAMP peptides disrupt microbial membranes and modulate host immune cell activity.
  • Leishmania parasites cause cutaneous infections, and their control involves host immune responses.

Purpose of the Study:

  • To investigate the role of CAMP in controlling cutaneous Leishmania infection.
  • To understand how CAMP influences host immune cell responses and parasite dissemination.
  • To explore the interaction between CAMP and Leishmania virulence factors.

Main Methods:

  • Utilized a CAMP knockout mouse model for Leishmania infection studies.
  • Assessed inflammatory infiltration, cytokine production (IL-10, IL-12, IFN-γ), and parasite dissemination.
  • Investigated the effect of Leishmania protease mutants on infection outcome.
  • Examined CAMP degradation by Leishmania protease in vitro.

Main Results:

  • CAMP-dependent inflammatory responses were observed in lesions and lymph nodes.
  • CAMP deficiency led to increased IL-10 receptor expression and IL-10 production, with reduced IL-12 and IFN-γ.
  • CAMP knockout mice exhibited exacerbated lesions and widespread parasite dissemination.
  • Leishmania protease degraded CAMP in vitro, suggesting a mechanism for immune evasion.

Conclusions:

  • CAMP plays a critical role in limiting Leishmania parasite dissemination and controlling infection severity.
  • Leishmania surface protease activity negatively regulates CAMP function, contributing to parasite survival.
  • This study reveals a complex interplay between CAMP, host immunity, and Leishmania virulence factors impacting infection outcomes.

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