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Anti-inflammatory responses and oxidative stress in Nippostrongylus brasiliensis-induced pulmonary inflammation

Kathryn S McNeil1, David P Knox, Lorna Proudfoot

  • 1School of Life Sciences, Napier University, Edinburgh, UK.

Parasite Immunology
|February 22, 2002
PubMed

Insights

Nippostrongylus brasiliensis larvae cause early lung damage but reduce inflammation. Despite initial injury, the host response shows decreased inflammatory cytokines and oxidative stress markers.

Area of Science:

  • Immunology
  • Parasitology
  • Pulmonology

Background:

  • Nippostrongylus brasiliensis (N. brasiliensis) is a nematode parasite that infects rodents.
  • Lung migration is a critical stage in the N. brasiliensis life cycle, involving host-parasite interactions within lung tissue.

Purpose of the Study:

  • To investigate the host immune response and tissue damage during the lung migration of L3 larvae of N. brasiliensis in rats.
  • To characterize early inflammatory and oxidative stress markers in bronchoalveolar lavage (BAL) fluid.

Main Methods:

  • Analysis of bronchoalveolar lavage (BAL) fluid at 24 hours, 72 hours, and 8 days post-infection (p.i.).
  • Measurement of protein, gamma-glutamyl transpeptidase, inflammatory cytokines (tumor necrosis factor alpha), oxidative stress markers (superoxide, lipid peroxidation), and nitric oxide metabolites.
  • Assessment of antioxidant enzyme activity (superoxide dismutase) and protein nitrosylation.

Main Results:

  • Early lung damage observed at 24 h p.i. with increased protein and gamma-glutamyl transpeptidase in BAL fluid.
  • Paradoxically, reduced inflammatory cell recruitment and decreased tumor necrosis factor alpha at 24 h p.i.
  • Modulation of oxidative stress with reduced superoxide production and lipid peroxidation, alongside increased superoxide dismutase activity.
  • Evidence of nitric oxide production and peroxynitrite formation throughout the infection.

Conclusions:

  • Despite initial lung epithelial and microvascular damage, N. brasiliensis L3 larvae appear to suppress the inflammatory response.
  • The parasite may employ mechanisms involving antioxidant systems and nitric oxide to modulate host inflammation during lung migration.

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