Common respiratory viruses in lower airways of patients with acute hypersensitivity pneumonitis

Common respiratory viruses in lower airways of patients with acute hypersensitivity pneumonitis
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DOI:
10.1164/ajrccm.159.4.9807085
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发表时间:
1999-04-01
影响因子:
24.7
通讯作者:
Cormier, Y
Cormier, Y
中科院分区:
医学1区
文献类型:
--
作者:
Dakhama, A;Hegele, RG;Cormier, Y

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过敏性肺炎 (HP) 是一种具有“流感样”症状的肺部疾病,是由于反复接触明确的非致病性抗原而引起的。本研究检查了 HP 患者的下呼吸道(可能发生过敏反应的部位)中是否存在呼吸道病毒。采用聚合酶链反应 (PCR) 方法检测急性 HP 患者和未接触过的健康志愿者的支气管肺泡灌洗 (BAL) 细胞中的 10 种常见呼吸道病毒。随后使用免疫细胞化学来定位 BAL 细胞内的病毒蛋白。 PCR 结果显示,甲型流感病毒是我们的研究患者(13 名中的 6 名)和对照受试者(6 名中的 2 名)的 BAL 细胞中最常检测到的病毒。在 13 名患者中的 9 名和 6 名对照受试者中的两名的肺泡巨噬细胞中检测到甲型流感蛋白。记录有甲型流感蛋白的患者的 BAL 细胞总数(而非淋巴细胞)高于无甲型流感蛋白的患者 (p = 0.017),并且与甲型流感阳性肺泡巨噬细胞的比例相关 (r = 0.7;p = 0.036)。该报告记录了急性 HP 患者下呼吸道中病毒的存在。这些发现可能暗示甲型流感在抗原暴露期间调节 HP 中具有潜在作用。
Hypersensitivity pneumonitis (HP), a lung disease with "flulike" symptoms, results from repeated exposures to well defined, nonpathogenic antigens, This study examined whether respiratory viruses are present in the lower airways, the likely site of hypersensitivity reaction, in patients with HP. The polymerase chain reaction (PCR) method was used to test for 10 common respiratory viruses in bronchoalveolar lavage (BAL) cells obtained from patients with acute HP and from unexposed healthy volunteers. Immunocytochemistry was subsequently used to localize viral proteins within BAL cells. The results of PCR showed that influenza A virus was the most frequently detected virus in the BAL cells of our study patients (six of 13) and control subjects (two of six). Influenza A proteins were detected within alveolar macrophages in nine of 13 patients and in two of six control subjects. The number of total BAL cells, but not lymphocytes, was higher in patients with documented influenza A proteins than in patients with no influenza A proteins (p = 0.017) and correlated with the proportion of influenza-A-positive alveolar macrophages (r = 0.7; p = 0.036). This report documents the presence of viruses in the lower airways of patients with acute HP. The findings may imply a potential role for influenza A in the modulation of HP during antigen exposure.