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Macrophages in the development of protective immunity against experimental Brugia malayi infection

R Gupta1, P Bajpai, L M Tripathi

  • 1Central Drug Research Institute, Lucknow-226001, India.

Parasitology
|October 9, 2004
PubMed

Insights

Resistant mastomys exhibit increased nitric oxide (NO) production, crucial for killing Brugia malayi larvae. Inhibiting NO in resistant hosts paradoxically enhances parasite survival, suggesting NO

Area of Science:

  • Immunology
  • Parasitology
  • Cell Biology

Background:

  • Lymphatic filariasis is a significant global health concern caused by Brugia malayi.
  • Macrophage function plays a critical role in host defense against parasitic infections.
  • Rodent models are essential for studying host-parasite interactions in lymphatic filariasis.

Purpose of the Study:

  • To compare macrophage function in Brugia malayi-susceptible and resistant rodent hosts.
  • To investigate the role of nitric oxide (NO) and other reactive oxygen species in parasite clearance.
  • To elucidate the mechanisms underlying differential host resistance to Brugia malayi infection.

Main Methods:

  • Isolation of peritoneal macrophages from infected mastomys (resistant) and gerbils (susceptible).
  • Assay of nitric oxide (NO), hydrogen peroxide (H2O2), superoxide (O2-), TNF-alpha, glutathione peroxidase, and reductase.
  • Administration of nitric oxide synthase (NOS) inhibitor aminoguanidine (AG) to assess NO's role.

Main Results:

  • Resistant mastomys showed significantly higher NO release compared to susceptible gerbils.
  • Aminoguanidine (AG) treatment suppressed NO production and increased parasite establishment in mastomys.
  • Hydrogen peroxide (H2O2) production was elevated in both species; higher glutathione levels protected mastomys.

Conclusions:

  • Peroxynitrite, formed by NO and superoxide, is likely involved in rapid killing of Brugia malayi larvae in resistant hosts.
  • Host resistance to Brugia malayi is associated with enhanced NO production by macrophages.
  • Tumor necrosis factor-alpha (TNF-alpha) appears to have an insignificant role in parasite establishment.

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