Watanabe A, Rossi P, Renzi P M, Xu L J, Guttmann R D, Martin J G
Meakins-Christie Laboratories, McGill University, Royal Victoria Hospital, Montreal, Quebec, Canada.
Am J Respir Crit Care Med. 1995 Jul;152(1):64-70. doi: 10.1164/ajrccm.152.1.7599864.
To evaluate the role of lymphocytes in the pathogenesis of allergic bronchoconstriction, we investigated whether allergic airway responses are adoptively transferred by antigen-primed lymphocytes in Brown Norway (BN) rats. Animals were actively sensitized to ovalbumin (OA) or sham sensitized, and 14 d later mononuclear cells (MNCs) were isolated from intrathoracic lymph nodes, passed through a nylon wool column, and transferred to naive syngeneic rats. Recipients were challenged with aerosolized OA or bovine serum albumin (BSA) (5% wt/vol) and analyzed for changes in lung resistance (RL), airway responsiveness to inhaled methacholine (MCh), and bronchoalveolar lavage (BAL) cells. Recipients of MNCs from sensitized rats responded to OA inhalation and exhibited sustained increases in RL throughout the 8-h observation period, but without usual early airway responses. Recipients of sham-sensitized MNCs or BSA-challenged recipients failed to respond to antigen challenge. At 32 h after OA exposure, airway responsiveness to MCh was increased in four of seven rats that had received sensitized MNCs (p = 0.035). BAL eosinophils increased at 32 h in the recipients of both sensitized and sham-sensitized MNCs. However, eosinophil numbers in BAL were inversely correlated with airway responsiveness in the recipients of sensitized MNCs (r = -0.788, p = 0.036). OA-specific immunoglobulin E (IgE) was undetectable by enzyme-linked immunosorbent assay (ELISA) or passive cutaneous anaphylaxis (PCA) in recipient rats following adoptive transfer. In conclusion, allergic late airway responses (LAR) and cholinergic airway hyperresponsiveness, but not antigen-specific IgE and early responses, were adoptively transferred by antigen-primed lymphocytes in BN rats.(ABSTRACT TRUNCATED AT 250 WORDS)
为评估淋巴细胞在过敏性支气管收缩发病机制中的作用，我们研究了在棕色挪威（BN）大鼠中，抗原致敏的淋巴细胞是否能引发过敏性气道反应。将动物主动致敏于卵清蛋白（OA）或进行假致敏，14天后从胸内淋巴结分离单核细胞（MNC），通过尼龙毛柱，然后转移至同基因未致敏大鼠。给受体大鼠雾化吸入OA或牛血清白蛋白（BSA）（5%重量/体积）进行激发，并分析肺阻力（RL）变化、气道对吸入乙酰甲胆碱（MCh）的反应性以及支气管肺泡灌洗（BAL）细胞情况。致敏大鼠的MNC受体对吸入OA有反应，在整个8小时观察期内RL持续升高，但无常见的早期气道反应。假致敏MNC受体或接受BSA激发的受体对抗原激发无反应。在OA暴露后32小时，接受致敏MNC的7只大鼠中有4只对MCh的气道反应性增加（p = 0.035）。致敏和假致敏MNC受体的BAL嗜酸性粒细胞在32小时均增加。然而，致敏MNC受体的BAL中嗜酸性粒细胞数量与气道反应性呈负相关（r = -0.788，p = 0.036）。过继转移后，在受体大鼠中通过酶联免疫吸附测定（ELISA）或被动皮肤过敏试验（PCA）均未检测到OA特异性免疫球蛋白E（IgE）。总之，在BN大鼠中，抗原致敏的淋巴细胞能引发过敏性迟发气道反应（LAR）和胆碱能性气道高反应性，但不能引发抗原特异性IgE和早期反应。（摘要截断于250字）
