title: Infection with Strongyloides venezuelensis induces transient airway eosinophilic inflammation, an increase in immunoglobulin E, and hyperresponsiveness in rats.
abstract: Infection by nematode parasites with a pulmonary migration in their life cycle and allergic asthma are two highly prevalent diseases in humans; therefore, one may expect both may occur concomitantly. There is a predominant and essential role of Th2 lymphocytes in the mechanisms underlying the control of parasite elimination as well as in the pathology observed in the asthmatic lung. The consequences of such situations have been explored, with controversial results, justifying the development of experimental models in which the relationship between allergic airway inflammation and helminth infection might be evaluated. The present work describes the inflammatory, humoral, and functional changes that occur in the lung of rats after single (subcutaneous inoculation of 1,500 L3 larvae) or multiple (five weekly subcutaneous inoculations of 1,500 L3 larvae) Strongyloides venezuelensis infections. The results show that the migration of S. venezuelensis larvae through the lungs of infected rats induces a local eosinophilic inflammation process which is mostly focal and parenchymal for rats infected a single time and which is peribronchial after multiple infections. The inflammatory process is accompanied by mucus hypersecretion, thickening of bronchial epithelial and muscle layers, and local increase in immunoglobulin E concentrations that peak after 5 to 7 days and are resolved after 12 days of single or multiple infections. The peak of lung immunopathologic changes observed in infected rats coincides with lung airway hyperresponsiveness (AHR), a key functional alteration in asthma. We propose that this experimental model is ideal to carry out further studies on immunoprotection against nematode infection versus immunopathology of allergic airway inflammation.
authors.affiliation: Department of Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Micheline R
authors.initials: MR
authors.lastname: Silveira
authors.forename: Kênia P
authors.initials: KP
authors.lastname: Nunes
authors.forename: Denise C
authors.initials: DC
authors.lastname: Cara
authors.forename: Danielle G
authors.initials: DG
authors.lastname: Souza
authors.forename: Ary
authors.initials: A
authors.lastname: Corrêa
authors.forename: Mauro M
authors.initials: MM
authors.lastname: Teixeira
authors.forename: Deborah
authors.initials: D
authors.lastname: Negrão-Corrêa
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology; D016535:Bronchial Hyperreactivity / Q000209:etiology*; D016207:Cytokines / Q000096:biosynthesis; D004802:Eosinophilia / Q000209:etiology*; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007249:Inflammation / Q000209:etiology*; D008168:Lung / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D013322:Strongyloidiasis / Q000150:complications / Q000276:immunology* / Q000473:pathology
chemical_list: D016207:Cytokines; D007073:Immunoglobulin E