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Published on: July 10, 2018
Complement C3a regulates late asthmatic response and airway hyperresponsiveness in mice
Nobuaki Mizutani1, Takeshi Nabe, Shin Yoshino
1Department of Pharmacology, Kobe Pharmaceutical University, Kobe, Japan. mizutani@kobepharma-u.ac.jp
Journal of Immunology (Baltimore, Md. : 1950)
|August 18, 2009
Summary
Complement C3a contributes to late-phase allergic asthma responses and airway hyperresponsiveness. Blocking its receptor reduced symptoms, suggesting C3a as a therapeutic target for asthma.
Area of Science:
- Immunology
- Pulmonology
- Pharmacology
Background:
- Allergic asthma is a chronic airway inflammation with biphasic obstruction and hyperresponsiveness.
- The role of complement component C3a in asthma pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the contribution of complement C3a to allergic asthma symptoms in a mouse model.
- To evaluate the therapeutic potential of C3a receptor antagonism.
Main Methods:
- Ovalbumin (OVA)-induced allergic asthma model in BALB/c mice.
- Administration of C3a receptor antagonist SB290157.
- Assessment of airway hyperresponsiveness, inflammatory cell infiltration, and cytokine expression (IL-1beta).
Main Results:
- OVA challenge induced biphasic airway obstruction, hyperresponsiveness, and increased C3a receptor expression.
- SB290157 significantly inhibited the late-phase response and airway hyperresponsiveness.
- Treatment reduced neutrophil infiltration and IL-1beta expression in the lungs.
Conclusions:
- C3a plays a significant role in the development of late asthmatic responses and airway hyperresponsiveness.
- C3a-mediated effects may involve neutrophil recruitment and IL-1beta production.
- C3a receptor antagonism presents a potential therapeutic strategy for allergic asthma.
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