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Changes in pulmonary function and parasite burden in rats infected with Strongyloides venezuelensis concomitant with induction of allergic airway inflammation.

Abstract
The prevalence of allergic diseases such as asthma has increased markedly over the past few decades. To evaluate the possible mutual influence of helminth infection and allergy, the combined effects of experimental allergic airway inflammation and infection with Strongyloides venezuelensis on various parasitological and inflammatory indices were evaluated in the rat. A challenge of immunized rats with aerosolized ovalbumin (OVA) resulted in eosinophilic inflammation that peaked 48 h after the challenge and was accompanied by airway hyperresponsiveness (AHR) to an intravenous acetylcholine challenge. S. venezuelensis infection concomitant with an OVA challenge of immunized rats resulted in prolonged pulmonary inflammation with increased eosinophil infiltration in bronchoalveolar lavage fluid but not in the lung tissue. These rats also showed a significant parasite burden reduction, especially during parasite migration through the lungs. However, the fecundity rates of worms that reached the intestine were similar in allergic and nonallergic animals. Despite airway inflammation, the increased responsiveness of the airways in the experimental asthma model was suppressed during parasite migration through the lungs (2 days). In contrast, parasite-induced AHR was unchanged 5 days after infection in immunized and challenged rats. In conclusion, infection with S. venezuelensis interfered with the onset of AHR following an antigen challenge of immunized rats. The ability of parasites to switch off functional airway responses is therapeutically relevant because we may learn from parasites how to modulate lung function and, hence, the AHR characteristic of asthmatic patients.
AuthorsDeborah Negrão-Corrêa, Micheline R Silveira, Cynthia M Borges, Danielle G Souza, Mauro M Teixeira
JournalInfection and immunity (Infect Immun) Vol. 71 Issue 5 Pg. 2607-14 (May 2003) ISSN: 0019-9567 [Print] United States
PMID12704135 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Interleukin-10
  • Immunoglobulin E
  • Ovalbumin
Topics
  • Animals
  • Asthma (etiology)
  • Bronchial Hyperreactivity (etiology)
  • Eosinophils (physiology)
  • Immunization
  • Immunoglobulin E (biosynthesis)
  • Interleukin-10 (biosynthesis)
  • Lung (physiopathology)
  • Male
  • Ovalbumin (immunology)
  • Rats
  • Rats, Wistar
  • Strongyloidiasis (complications, immunology, parasitology)

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