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08:33
A Method for Generating Pulmonary Neutrophilia Using Aerosolized Lipopolysaccharide
Published on: December 15, 2014
Neutrophilic inflammation in severe asthma
Kazuyuki Nakagome1, Sho Matsushita, Makoto Nagata
1Department of Respiratory Medicine, Saitama Medical University, Iruma-gun, Saitama, Japan. nakagomek-tky@umin.ac.jp
International Archives of Allergy and Immunology
|May 26, 2012
Summary
Dopamine D1-like receptor antagonists may treat severe asthma by inhibiting T helper 17 cells and neutrophil airway inflammation. This offers a new therapeutic strategy for corticosteroid-resistant asthma.
Area of Science:
- Immunology
- Pulmonology
- Pharmacology
Background:
- Neutrophil infiltration and Interleukin-8 (IL-8) upregulation are implicated in severe asthma pathogenesis.
- IL-8-stimulated neutrophils can enhance eosinophil migration, contributing to airway inflammation and potential corticosteroid resistance.
- T helper 17 (Th17) cells are suspected to be involved in IL-8 upregulation in severe asthma.
Purpose of the Study:
- To investigate the role of dopamine in Th17 differentiation and its impact on neutrophilic airway inflammation.
- To evaluate the therapeutic potential of dopamine D1-like receptor (D1-like-R) antagonists in a mouse model of asthma.
Main Methods:
- Investigated dopamine's effect on Th17 differentiation via D1-like-R.
- Utilized a D1-like-R antagonist to assess its effects in ovalbumin (OVA)-induced neutrophilic airway inflammation in DO11.10 mice.
- Assessed Th17-mediated immune responses and airway inflammation markers.
Main Results:
- Dopamine was found to induce Th17 differentiation through D1-like-R.
- A D1-like-R antagonist significantly suppressed OVA-induced neutrophilic airway inflammation.
- The suppression of inflammation was linked to the inhibition of Th17-mediated immune responses.
Conclusions:
- Dopamine D1-like-R antagonists show promise for treating Th17-mediated, neutrophil-dominant severe asthma.
- Targeting the dopamine-D1-like-R-Th17 axis offers a potential therapeutic strategy for corticosteroid-resistant asthma.
- Further research is needed to elucidate mechanisms for controlling neutrophilic inflammation in asthma.
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