title: Modulation of murine experimental asthma by Ascaris suum components.
abstract: BACKGROUND
  We have recently isolated two distinct components from Ascaris suum adult worms with different effects on the immune system: the allergenic protein of A. suum (APAS-3), which induces IgE antibody production, and suppressive protein of A. suum (PAS-1), which inhibits humoral and cellular immune responses induced by unrelated antigens. In this study, we investigated the immunomodulatory effect of PAS-1 on a murine model of asthma induced by APAS-3.
  
  
  METHODS
  BALB/c mice were immunized twice with APAS-3 or APAS-3 plus PAS-1 by the intraperitoneal and subcutaneous route (on days 0 and 7) and challenged twice with the same antigens intranasally (days 14 and 21). Two days after the last challenge, the allergic airway inflammation was evaluated by cellular migration, eosinophil peroxidase (EPO) activity, cytokine and chemokine production and pulmonary mechanical parameters.
  
  
  RESULTS
  The allergenic properties of APAS-3 were confirmed by the stimulation of anaphylactic IgE and IgG1 antibody production and eosinophilic airway inflammation and hyper-responsiveness. On the other hand, PAS-1-treated mice showed a marked suppression of cellular migration and EPO activity that correlated well with a significant reduction in the levels of IL-4, IL-5, eotaxin and RANTES in the bronchoalveolar lavage (BAL) fluid. In contrast, considerable amounts of IL-10 were observed in the BAL fluid of PAS-1-treated mice. Airway hyper-responsiveness was obtained in APAS-3-immunized mice, but the conductance of the respiratory system was restored to normal values in the presence of PAS-1.
  
  
  CONCLUSIONS
  These results indicate that A. suum allergenic protein APAS-3 induces a T helper 2-type immune response and, consequently, eosinophilic airway inflammation and hyper-responsiveness. Moreover, the modulatory protein PAS-1 has a marked suppressive effect on this response, and the inhibition of cytokine (IL-4, IL-5) and chemokine (eotaxin and RANTES) release, probably because of the presence of IL-10, may contribute to this effect.
authors: Laboratory of Immunopathology, Butantan Institute, São Paulo, Brazil.
authors: D M
authors: DM
authors: Itami
authors: T M
authors: TM
authors: Oshiro
authors: C A
authors: CA
authors: Araujo
authors: A
authors: A
authors: Perini
authors: M A
authors: MA
authors: Martins
authors: M S
authors: MS
authors: Macedo
authors: M F
authors: MF
authors: Macedo-Soares
mesh_terms: D000485:Allergens / Q000276:immunology; D000707:Anaphylaxis / Q000276:immunology; D000818:Animals; D017165:Ascaris suum / Q000276:immunology*; D001249:Asthma / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002464:Cell Migration Inhibition; D054413:Chemokine CCL11; D018946:Chemokine CCL5 / Q000276:immunology; D019742:Chemokines, CC / Q000276:immunology; D002631:Chemotactic Factors, Eosinophil / Q000276:immunology; D004195:Disease Models, Animal; D047209:Eosinophil Peroxidase / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D005260:Female; D015801:Helminth Proteins / Q000276:immunology*; D007073:Immunoglobulin E / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D007378:Interleukins / Q000276:immunology; D008168:Lung / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000485:Allergens; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D015801:Helminth Proteins; D007074:Immunoglobulin G; D007378:Interleukins; D007073:Immunoglobulin E; D047209:Eosinophil Peroxidase