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A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
Published on: April 13, 2010
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Th9 cells induce steroid-resistant bronchial hyperresponsiveness in mice
Mayumi Saeki1, Osamu Kaminuma2, Tomoe Nishimura1
1Allergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Summary
Dexamethasone (Dex) did not affect airway inflammation in mice transferred with Th9 cells, unlike Th2 cells. This suggests Th9 cells may contribute to steroid-resistant asthma, a significant clinical challenge.
Area of Science:
- Immunology
- Respiratory Medicine
- Pharmacology
Background:
- Corticosteroid therapy is often ineffective for severe asthma.
- Th9 cells, like Th2 cells, contribute to airway inflammation and hyperresponsiveness.
- The impact of steroids on Th9 cell-mediated responses is not well understood.
Purpose of the Study:
- To investigate the effect of dexamethasone (Dex) on antigen-induced airway inflammation mediated by Th9 cells.
- To compare the sensitivity of Th9 and Th2 cell responses to steroid treatment.
Main Methods:
- Ovalbumin (OVA)-specific Th2 and Th9 cells were generated and transferred to mice.
- Mice were challenged with OVA and treated with Dex.
- Airway inflammation and responsiveness to methacholine were assessed.
Main Results:
- Dex treatment reduced airway inflammation and hyperresponsiveness in Th2 cell-transferred mice.
- In Th9 cell-transferred mice, Dex did not affect airway inflammation or hyperresponsiveness.
- Antigen-induced lung infiltration of Th2 cells was suppressed by Dex, but Th9 cell infiltration was not.
Conclusions:
- Th9-mediated airway inflammation is resistant to dexamethasone treatment.
- Th9 cells may play a role in the development of steroid-resistant asthma.
