Cytokines derived from alveolar macrophages induce fever after bronchoscopy and bronchoalveolar lavage
Cytokines derived from alveolar macrophages induce fever after bronchoscopy and bronchoalveolar lavage
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DOI：
10.1164/ajrccm.155.5.9154894
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发表时间：
1997-05-01
影响因子：
24.7
通讯作者：
Witt, C
中科院分区：
文献类型：
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作者：
Krause, A;Hohberg, B;Witt, C
多达三分之一的患者在纤维支气管镜检查（FOE）和支气管肺泡灌洗（BAL）后出现发烧和流感样症状，原因尚不清楚。本研究的目的是调查介导这些副作用的因素。连续 50 名患有各种肺部疾病的患者入组，这些患者在没有进一步干预的情况下接受了 FOE (n = 30) 或联合 BAL (n = 20)。促炎细胞因子IL-1β、IL-6和TNF-α的血清水平通过ELISA在手术之前(t(0))、手术后(t(1))和手术后6小时(t(2))测定。同时，在 t(2) 时抽取血培养物。在 t(0) 和 t(1) 时，通常只能检测到较低的细胞因子浓度。然而，在 t(2) 时，发现细胞因子水平显着增加。 BAL 后患者的 IL-6 和 TNF-α 显着高于 FOE 后患者。将发烧患者 (n = 12) 与未发烧患者 (n = 38) 进行比较，无论进行何种内窥镜手术，在发烧患者中均检测到所有三种细胞因子均显着增加，且显着高于不发烧患者。在FOE组中，只有通过支气管镜工作通道向气道推注丙胺卡因进行局部麻醉的患者出现发热且IL-6和IL-β升高，而通过吸入丙胺卡因气雾剂进行麻醉的患者仍然无发热，并且仅出现轻微的IL-6升高。 t(2) 时的 IL-6 值与 BAL 肺泡巨噬细胞数量之间存在高度显着相关性 (r = 0.98)。所有血培养物均保持无菌。这些结果表明，FOE 和 BAL 后的发热是由促炎性细胞因子引起的，这些细胞因子源自通过将液体滴入气道而激活的肺泡巨噬细胞。
As much as one-third of patients develop fever and flu-like symptoms after fiberoptic bronchoscopy (FOE) and bronchoalveolar lavage (BAL) for yet unknown reasons. The aim of the present study was to investigate factors mediating these side effects. Fifty consecutive patients with various pulmonary diseases who underwent FOE without further interventions (n = 30) or combined with BAL (n = 20) were enrolled. Serum levels of the proinflammatory cytokines IL-1 beta, IL-6, and TNF-alpha were determined directly prior to (t(0)), directly after (t(1)), and 6 h after (t(2)) the procedures by ELISA. In parallel, blood cultures were drawn at t(2). At t(0) and t(1), generally only low cytokine concentrations could be detected. At t(2), however, significant increases of cytokine levels were found. IL-6 and TNF-alpha were significantly higher in patients after BAL than in patients after FOE. Comparing patients who developed fever (n = 12) with those who did not (n = 38), irrespective of the endoscopic procedures performed, dramatic increases of all three cytokines were detected in febrile patients that were significantly higher than in patients without fever. In the FOE group only patients who received local anesthesia by prilocaine bolus injection into the airways via the working channel of the bronchoscope developed fever and increases of IL-6 and IL-beta, whereas patients anaesthetized by inhalation of a prilocaine aerosol remained afebrile and had slight IL-6 increases only. There was a highly significant correlation between IL-6 values at t(2) and the number of BAL alveolar macrophages (r = 0.98). All blood cultures remained sterile. These results indicate that fever after FOE and BAL is induced by proinflammatory cytokines derived from alveolar macrophages activated by instillation of fluid into the airways.