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IL-12p40 is essential for the down-regulation of airway hyperresponsiveness in a mouse model of bronchial asthma with prolonged antigen exposure.
Clin Exp Allergy. 2009 Feb; 39(2):290-8.CE

Abstract

BACKGROUND

We previously reported a mouse model of bronchial asthma showing eosinophilic inflammation, but not airway hyperresponsiveness (AHR), after prolonged antigen exposure. This model showed an increase of IL-12 in the lung.

OBJECTIVE

The aim of this study was to investigate the role of IL-12p40 in a murine asthma model with prolonged antigen exposures.

METHODS

An ovalbumin (OVA)-induced asthma model was first established in wild-type (WT) and IL-12p40-deficient (IL-12p40(-/-)) mice. Both strains of mice were further exposed to either OVA (prolonged exposure group) or phosphate-buffered saline (positive control group) 3 days per week for 3 weeks. During week 4, both groups of mice were given a final challenge with OVA.

RESULTS

Prolonged antigen exposures resulted in marked suppression of airway eosinophilia in both WT and IL-12p40(-/-) mice. However, AHR persisted in IL-12p40(-/-) but not in WT mice. There were no significant differences of IL-5, IL-13 or IFN-gamma levels in bronchoalveolar lavage fluid between WT and IL-12p40(-/-) mice. The hydroxyproline content of the lung and peribronchial fibrosis were, however, significantly increased in IL-12p40(-/-) mice.

CONCLUSION

The results suggest that endogenous IL-12p40 is essential for inhibition of AHR and peribronchial fibrosis, but not eosinophilic inflammation, in a murine asthma model with prolonged antigen exposures.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Onari Y
Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Yokoyama A
No affiliation info available
Haruta Y
No affiliation info available
Nakashima T
No affiliation info available
Iwamoto H
No affiliation info available
Hattori N
No affiliation info available
Kohno N
No affiliation info available

MeSH

Administration, InhalationAnimalsAsthmaBronchial HyperreactivityBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalDown-RegulationEosinophilsFemaleImmune ToleranceInterleukin-12 Subunit p40LeukocytesLungMaleMiceMice, Inbred C57BLMice, KnockoutOvalbuminRespiratory Function Tests

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19032358

Citation

Onari, Y, et al. "IL-12p40 Is Essential for the Down-regulation of Airway Hyperresponsiveness in a Mouse Model of Bronchial Asthma With Prolonged Antigen Exposure." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 39, no. 2, 2009, pp. 290-8.
Onari Y, Yokoyama A, Haruta Y, et al. IL-12p40 is essential for the down-regulation of airway hyperresponsiveness in a mouse model of bronchial asthma with prolonged antigen exposure. Clin Exp Allergy. 2009;39(2):290-8.
Onari, Y., Yokoyama, A., Haruta, Y., Nakashima, T., Iwamoto, H., Hattori, N., & Kohno, N. (2009). IL-12p40 is essential for the down-regulation of airway hyperresponsiveness in a mouse model of bronchial asthma with prolonged antigen exposure. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 39(2), 290-8. https://doi.org/10.1111/j.1365-2222.2008.03131.x
Onari Y, et al. IL-12p40 Is Essential for the Down-regulation of Airway Hyperresponsiveness in a Mouse Model of Bronchial Asthma With Prolonged Antigen Exposure. Clin Exp Allergy. 2009;39(2):290-8. PubMed PMID: 19032358.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IL-12p40 is essential for the down-regulation of airway hyperresponsiveness in a mouse model of bronchial asthma with prolonged antigen exposure. AU - Onari,Y, AU - Yokoyama,A, AU - Haruta,Y, AU - Nakashima,T, AU - Iwamoto,H, AU - Hattori,N, AU - Kohno,N, Y1 - 2008/11/17/ PY - 2008/11/27/pubmed PY - 2009/3/31/medline PY - 2008/11/27/entrez SP - 290 EP - 8 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 39 IS - 2 N2 - BACKGROUND: We previously reported a mouse model of bronchial asthma showing eosinophilic inflammation, but not airway hyperresponsiveness (AHR), after prolonged antigen exposure. This model showed an increase of IL-12 in the lung. OBJECTIVE: The aim of this study was to investigate the role of IL-12p40 in a murine asthma model with prolonged antigen exposures. METHODS: An ovalbumin (OVA)-induced asthma model was first established in wild-type (WT) and IL-12p40-deficient (IL-12p40(-/-)) mice. Both strains of mice were further exposed to either OVA (prolonged exposure group) or phosphate-buffered saline (positive control group) 3 days per week for 3 weeks. During week 4, both groups of mice were given a final challenge with OVA. RESULTS: Prolonged antigen exposures resulted in marked suppression of airway eosinophilia in both WT and IL-12p40(-/-) mice. However, AHR persisted in IL-12p40(-/-) but not in WT mice. There were no significant differences of IL-5, IL-13 or IFN-gamma levels in bronchoalveolar lavage fluid between WT and IL-12p40(-/-) mice. The hydroxyproline content of the lung and peribronchial fibrosis were, however, significantly increased in IL-12p40(-/-) mice. CONCLUSION: The results suggest that endogenous IL-12p40 is essential for inhibition of AHR and peribronchial fibrosis, but not eosinophilic inflammation, in a murine asthma model with prolonged antigen exposures. SN - 1365-2222 UR - https://www.unboundmedicine.com/medline/citation/19032358/IL_12p40_is_essential_for_the_down_regulation_of_airway_hyperresponsiveness_in_a_mouse_model_of_bronchial_asthma_with_prolonged_antigen_exposure_ DB - PRIME DP - Unbound Medicine ER -