Crummy Fionnuala, Livingston Mark, Ennis Madeleine, Heaney Liam G
Respiratory Research Group, Inflammation Research Centre, Department of Medicine, Queen's University of Belfast, Ireland.
J Allergy Clin Immunol. 2004 Jul;114(1):34-9. doi: 10.1016/j.jaci.2004.03.006.
Adenosine 5'-monophosphate (AMP) has been shown to cause bronchoconstriction in atopic subjects but to have no effect on nonatopic nonasthmatic subjects. Endobronchial AMP challenge has previously been shown to cause mast cell mediator release in asthmatic subjects, but it is unknown whether a similar response occurs in atopic nonasthmatic and nonatopic nonasthmatic control subjects who have no response to inhalation AMP challenge.
This study examined the change in mast cell-derived products after endobronchial saline challenge and AMP challenge in subjects with and without a positive inhalation response to AMP.
Inhalation challenge with AMP challenge was performed in normal, atopic nonasthmatic, and atopic asthmatic subjects. Levels of mast cell mediators were measured after endobronchial adenosine challenge and after placebo endobronchial saline challenge.
There were significant increases in histamine, tryptase, protein, and prostaglandin D2 levels (P=.02, P=.02, P=.01, and P=.01, respectively) after AMP challenge compared with after saline challenge in nonatopic nonasthmatic subjects. There was no significant increase in any mediator in either of the other 2 groups.
This study suggests dissociation between mediator release and bronchoconstriction in response to AMP.
已证实5'-单磷酸腺苷(AMP)可使特应性受试者发生支气管收缩,但对非特应性非哮喘受试者无影响。先前已表明支气管内AMP激发可导致哮喘受试者肥大细胞介质释放,但尚不清楚在对吸入AMP激发无反应的特应性非哮喘和非特应性非哮喘对照受试者中是否会出现类似反应。
本研究检测了对AMP吸入反应呈阳性和阴性的受试者在支气管内盐水激发和AMP激发后肥大细胞衍生产物的变化。
对正常、特应性非哮喘和特应性哮喘受试者进行AMP吸入激发。在支气管内腺苷激发后和安慰剂支气管内盐水激发后测量肥大细胞介质水平。
与盐水激发后相比,非特应性非哮喘受试者在AMP激发后组胺、类胰蛋白酶、蛋白质和前列腺素D2水平显著升高(分别为P = 0.02、P = 0.02、P = 0.01和P = 0.01)。其他两组中任何介质均无显著升高。
本研究提示在对AMP的反应中介质释放与支气管收缩之间存在分离。