Modulation of murine experimental asthma by Ascaris suum components
- 6 July 2005
- journal article
- Published by Wiley in Clinical and Experimental Allergy
- Vol. 35 (7), 873-879
- https://doi.org/10.1111/j.1365-2222.2005.02268.x
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. Conclusion 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.Keywords
This publication has 31 references indexed in Scilit:
- IL-4 and IL-10 are essential for immunosuppression induced by high molecular weight proteins from Ascaris suumCytokine, 2004
- Immunoglobulin E is not required for but enhances airway inflammation and hyperresponsivenessAllergy, 2003
- The Role of IL-10 and TGF-β in the Differentiation and Effector Function of T Regulatory CellsInternational Archives of Allergy and Immunology, 2002
- CCL Chemokines and asthmaImmunology Today, 2000
- Airway eosinophilia is not a requirement for allergen‐induced airway hyperresponsivenessClinical and Experimental Allergy, 2000
- Protective effect of inhaled lysine acetylsalicylate on allergen-induced early and late asthmatic reactionsJournal of Allergy and Clinical Immunology, 1997
- Interleukin‐5 and eosinophils induce airway damage and bronchial hyperreactivity during allergic airway inflammation in BALB/c miceImmunology & Cell Biology, 1997
- Cooperation between interleukin-5 and the chemokine eotaxin to induce eosinophil accumulation in vivo.The Journal of Experimental Medicine, 1995
- Isolation of Ascaris suum Components Which Suppress IgE Antibody ResponsesInternational Archives of Allergy and Immunology, 1992
- Homologous and heterologous passive cutaneous anaphylactic activity of mouse antisera during the course of immunizationLife Sciences, 1969