Trezena Aryene Goes, da Silva Zilma Lucia, Oliveira-Filho Ricardo Martins, Damazo Amilcar Sabino, Straus Anita Hilda, Takahashi Helio Kiyoshi, Oliani Sonia Maria, de Lima Wothan Tavares
Laboratory of Immunogenetics and Laboratory of Anaerobic Vaccines, Butantan Institute, São Paulo, Brazil.
Mediators Inflamm. 2003 Aug;12(4):237-46. doi: 10.1080/09629350310001599684.
Rat trachea display a differential topographical distribution of connective tissue mast cells (CTMC) and mucosal mast cells (MMC) that may imply regional differences in the release of allergic mediators such as tumor necrosis factor-alpha (TNF-alpha) and eicosanoids.
To evaluate the role of CTMC and MMC for release of TNF-alpha and eicosanoids after allergenic challenge in distinct segments of rat trachea.
Proximal trachea (PT) and distal trachea (DT) from ovalbumin (OVA)-sensitized rats, treated or not with compound 48/80 (48/80) or dexamethasone, were incubated in culture medium. After OVA challenge, aliquots were collected to study release of TNF-alpha and eicosanoids.
Release of TNF-alpha by PT upon OVA challenge peaked at 90 min and decayed at 6 and 24 h. Release from DT peaked at 30-90 min and decayed 6 and 24 h later. When CTMC were depleted with 48/80, OVA challenge exacerbated the TNF-alpha release by PT at all time intervals, while DT exacerbated TNF-alpha levels 6 and 24 h later only. Dexamethasone reduced TNF-alpha production after 90 min of OVA challenge in PT and at 3 and 6h in DT. OVA challenge increased prostaglandin D2) in DT and leukotriene B4 in both segments but did not modify prostaglandin E2 and leukotriene C4 release.
OVA challenge induces TNF-alpha release from MMC, which is negatively regulated by CTMC. The profile of TNF-alpha and eicosanoids depends on the time after OVA challenge and of the tracheal segment considered.
大鼠气管中结缔组织肥大细胞（CTMC）和黏膜肥大细胞（MMC）呈现出不同的地形分布，这可能意味着在诸如肿瘤坏死因子-α（TNF-α）和类花生酸等过敏介质释放方面存在区域差异。
评估CTMC和MMC在大鼠气管不同节段变应原激发后释放TNF-α和类花生酸中的作用。
将来自卵清蛋白（OVA）致敏大鼠的近端气管（PT）和远端气管（DT），用或不用化合物48/80（48/80）或地塞米松处理后，在培养基中孵育。OVA激发后，收集等分试样以研究TNF-α和类花生酸的释放。
OVA激发后PT释放TNF-α在90分钟时达到峰值，并在6小时和24小时时下降。DT释放的TNF-α在30 - 90分钟时达到峰值，并在6小时和24小时后下降。当用48/80耗尽CTMC时，OVA激发在所有时间间隔均加剧了PT的TNF-α释放，而DT仅在6小时和24小时后加剧了TNF-α水平。地塞米松在OVA激发90分钟后降低了PT中的TNF-α产生，并在DT中在3小时和6小时时降低了TNF-α产生。OVA激发增加了DT中的前列腺素D2以及两个节段中的白三烯B4，但未改变前列腺素E2和白三烯C4的释放。
OVA激发诱导MMC释放TNF-α，而CTMC对其起负调节作用。TNF-α和类花生酸的释放情况取决于OVA激发后的时间以及所考虑的气管节段。
