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Cloned Th cells confer eosinophilic inflammation and bronchial hyperresponsiveness
1Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan. osamu@liai.org
International Archives of Allergy and Immunology
|May 4, 1999
Summary
T helper (Th) cells are sufficient to cause airway eosinophilic inflammation and bronchial hyperresponsiveness (BHR). Downregulating interleukin-5 (IL-5) production may be a promising treatment for asthma.
Area of Science:
- Immunology
- Respiratory Medicine
- Allergy Research
Background:
- T helper (Th) cells and their cytokines are crucial in eosinophilic inflammation.
- The specific role of Th cells in initiating airway eosinophilic inflammation requires further clarification.
Purpose of the Study:
- To investigate if T helper cells alone are sufficient to induce airway eosinophilic inflammation.
- To explore the potential of targeting IL-5 for asthma treatment.
Main Methods:
- Ovalbumin-reactive murine Th cell clones were established and transferred into naive mice.
- Antigen inhalation was used to induce inflammation, followed by analysis of bronchoalveolar lavage fluid (BALF) and lung pathology.
- The effects of anti-IL-5 antibody, dexamethasone, and cyclosporin A were evaluated.
Main Results:
- Infused Th cells migrated to the lungs, leading to eosinophilic infiltration and increased BALF eosinophil peroxidase activity upon antigen challenge.
- Asthma-like pathology, including epithelial damage and mucus production, was observed.
- Bronchial hyperresponsiveness (BHR) was induced and correlated with eosinophil counts.
- Anti-IL-5 antibody treatment abrogated the inflammatory response, while dexamethasone and cyclosporin A suppressed Th cell cytokine production, BALF eosinophilia, and BHR.
Conclusions:
- Monoclonal T helper cells are sufficient to cause airway eosinophilia and BHR.
- Targeting IL-5 production presents a potential therapeutic strategy for managing bronchial asthma.