Anaphylatoxin C3a receptors in asthma.
Anaphylatoxin C3a receptors in asthma.
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DOI：
10.1186/1465-9921-6-19
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发表时间：
2005-02-21
影响因子：
5.8
通讯作者：
Panettieri RA Jr
中科院分区：
文献类型：
--
作者：
Ali H;Panettieri RA Jr
补体系统构成先天免疫的中心核心，但也介导各种炎症反应。过敏毒素C3a是补体激活的副产物，长期以来一直被认为可以激活肥大细胞、嗜碱性粒细胞和嗜酸性粒细胞，并导致平滑肌收缩。然而，C3a在过敏性哮喘发病机制中的作用尚不清楚。在这篇综述中，我们研究了C3a在促进哮喘中的作用。在过敏原攻击后，C3a在哮喘患者的肺中产生，但不是健康受试者。此外，在小鼠肺部炎症和呼吸道高反应性模型中，C3a生成或G蛋白偶联受体缺乏可消除变应原诱导的反应。此外，在致敏后、变应原激发前抑制补体激活或给予C3a受体小分子抑制剂可抑制呼吸道反应。在细胞水平上，C3a刺激强大的肥大细胞脱颗粒，这种脱颗粒在细胞与呼吸道平滑肌(ASM)细胞接触后大大增强。因此，C3a可能主要通过调节肥大细胞与ASM细胞的相互作用而在哮喘发病中发挥重要作用。
The complement system forms the central core of innate immunity but also mediates a variety of inflammatory responses. Anaphylatoxin C3a, which is generated as a byproduct of complement activation, has long been known to activate mast cells, basophils and eosinophils and to cause smooth muscle contraction. However, the role of C3a in the pathogenesis of allergic asthma remains unclear. In this review, we examine the role of C3a in promoting asthma. Following allergen challenge, C3a is generated in the lung of subjects with asthma but not healthy subjects. Furthermore, deficiency in C3a generation or in G protein coupled receptor for C3a abrogates allergen-induced responses in murine models of pulmonary inflammation and airway hyperresponsiveness. In addition, inhibition of complement activation or administration of small molecule inhibitors of C3a receptor after sensitization but before allergen challenge inhibits airway responses. At a cellular level, C3a stimulates robust mast cell degranulation that is greatly enhanced following cell-cell contact with airway smooth muscle (ASM) cells. Therefore, C3a likely plays an important role in asthma primarily by regulating mast cell-ASM cell interaction.
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影响因子：
4.4
作者：
Ali, H;Ahamed, J;Patel, DD
通讯作者：
Patel, DD
影响因子：
24.3
作者：
Carroll, NG;Mutavdzic, S;James, AL
通讯作者：
James, AL
DOI：
10.1165/ajrcmb.26.4.4681
发表时间：
2002-04-01
影响因子：
6.4
作者：
Ammit, AJ;Lazaar, AL;Panettieri, RA
通讯作者：
Panettieri, RA
影响因子：
4.4
作者：
Baelder, R;Fuchs, B;Braun, A
通讯作者：
Braun, A
DOI：
10.1073/pnas.87.17.6813
发表时间：
1990-09-01
影响因子：
11.1
作者：
BISCHOFF, SC;DEWECK, AL;DAHINDEN, CA
通讯作者：
DAHINDEN, CA