Inflammation in Mice Hyperresponsiveness via Neutrophilic Asthmatic Response and Airway Critical Role in an IgE-Mediated Late-Phase Complement C3a-Induced IL-17 Plays a
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Complement C3a regulates late asthmatic response and airway hyperresponsiveness in mice.
Allergic asthma is a chronic inflammatory disorder of the airways characterized by biphasic airway obstruction and airway hyperresponsiveness. In this study, we attempted to elucidate the contribution of the complement C3a to these asthmatic symptoms. BALB/c mice sensitized by i.p. injections of OVA plus alum were challenged with OVA intratracheally four times. The fourth challenge caused a bip...
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RATIONALE Reports from our laboratory, as well as those from others, have documented the importance of complement activation, the C3a anaphylatoxin, and its receptor, C3aR, in promoting Th2 effector functions in a mouse model of bronchopulmonary allergy. Although deficiency in the fifth complement component (C5) has been linked to enhanced airway hyperresponsiveness in mice, the contribution of...
متن کاملAbsence of the complement anaphylatoxin C3a receptor suppresses Th2 effector functions in a murine model of pulmonary allergy.
Asthma is a chronic inflammatory disease of the lung resulting in airway obstruction. The airway inflammation of asthma is strongly linked to Th2 lymphocytes and their cytokines, particularly IL-4, IL-5, and IL-13, which regulate airway hyperresponsiveness, eosinophil activation, mucus production, and IgE secretion. Historically, complement was not thought to contribute to the pathogenesis of a...
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IL-17A induces the release of pro-inflammatory cytokines and of reactive oxygen species which could lead to neutrophilic inflammation. We determined the role of IL-17 receptor (IL-17R) signalling in oxidant-induced lung emphysema and airway hyperresponsiveness. IL-17R(-/-) and wild-type C57/BL6 mice were exposed to ozone (3 ppm; 3 hours) for 12 times over 6 weeks. Bronchial responsiveness to ac...
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Thus the pathophysiology of allergic asthma is traditionally explained by mast celland/or Th2 cell-mediated airway inflammation, which is a manifestation of the acquired immune response. On the other hand, recent studies have identified various other important molecules associated with phenotypes of asthma, including tumor necrosis factor (TNF)[2, 3] , thymic stromal lymphoprotein [4, 5] , inte...
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