Phospholipase A(2) and arachidonate increase in bronchoalveolar lavage fluid after inhaled antigen challenge in asthmatics

Phospholipase A(2) and arachidonate increase in bronchoalveolar lavage fluid after inhaled antigen challenge in asthmatics
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DOI:
10.1164/ajrccm.155.2.9032172
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发表时间:
1997-02-01
影响因子:
24.7
通讯作者:
Bass, DA
Bass, DA
中科院分区:
医学1区
文献类型:
--
作者:
Bowton, DL;Seeds, MC;Bass, DA

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磷脂酶A(2)(PLA(2))水解磷脂,导致脂肪酸(包括花生四烯酸(AA)和溶血磷脂)的释放。反过来,AA作为白三烯合成的底物,可引起支气管收缩和气道水肿,似乎是临床哮喘的重要介质。此外,溶血磷脂可能具有细胞毒性和/或损害表面活性剂的功能。我们检测了16名过敏性哮喘受试者抗原激发后分泌型PLA(2)(sPLA(2))和AA释放到气道中的情况。哮喘受试者在吸入抗原激发前后接受支气管肺泡灌洗(BAL)支气管镜检查;此外,在10名对照受试者中进行单次BAL,不吸入抗原。在激发后4 h(n = 7)、迟发哮喘反应(LAR)时间(n = 5)或24 h(n = 4)获得BAL。在基线时,正常和哮喘受试者之间的BALF(BALF)sPLA(2)活性或AA浓度均无差异。抗原攻击后sPLA(2)和AA均增加(分别为p < 0.01和p <0.05)。这些变化在攻击后4小时最显著(两者p < 0.03)。sPLA(2)可能在哮喘患者AA的产生中起重要作用。
Phospholipases A(2) (PLA(2)) hydrolyze phospholipids resulting in the release of fatty acids including arachidonic acid (AA) and lysophospholipids. AA, in turn, serves as a substrate for the synthesis of leukotrienes which can cause bronchoconstriction and airways edema and appear to be important mediators of clinical asthma. Further, lysophospholipids may be cytotoxic and/or impair the function of surfactant. We examined the release of secretory PLA(2) (sPLA(2)) and AA into the airways after antigen challenge in 16 subjects with allergic asthma. Asthmatic subjects underwent bronchoscopy with bronchoalveolar lavage (BAL) before and after inhaled antigen challenge; in addition, a single BAL, without inhaled antigen, was performed in 10 control subjects. BAL was obtained at 4 h (n = 7), the time of the late asthmatic response (LAR) (n = 5), or 24 h (n = 4) after challenge. There was no difference between normal and asthmatic subjects in either BAL fluid (BALF) sPLA(2) activity or AA concentration at baseline. Both sPLA(2) and AA increased after antigen challenge (p < 0.01 and 0.05, respectively). These changes were most marked 4 h after challenge (p < 0.03 for both). sPLA(2) may play an important role in the generation of AA in patients with asthma.