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过敏性肺炎中CCL18/DC-CK-1/PARC的上调

CCL18/DC-CK-1/PARC up-regulation in hypersensitivity pneumonitis.

作者信息

Pardo A, Smith K M, Abrams J, Coffman R, Bustos M, McClanahan T K, Grein J, Murphy E E, Zlotnik A, Selman M

机构信息

Facultad de Ciencias, Universidad Nacional Autónoma de México.

出版信息

J Leukoc Biol. 2001 Oct;70(4):610-6.

Abstract

Hypersensitivity pneumonitis (HP) is a lung inflammatory disorder characterized by accumulation of T lymphocytes. However, the mechanisms implicated in this process remain undefined. We examined the expression of dendritic cell (DC)-derived CC chemokine 1 (CK1)/CCL18, a chemokine putatively involved in naive T cell recruitment, in lungs from 10 patients with HP, 9 patients with idiopathic pulmonary fibrosis (IPF), and 20 healthy lungs. CCL18 was measured by real-time quantitative PCR and localized in lungs by in situ hybridization and immunohistochemistry. CCL18 expression was significantly increased in lungs affected by HP in comparison with lungs affected by IPF (2,085+/-393 vs. 1,023+/-110; P<0.05) and controls (2,085+/-393 vs. 467+/-94; P<0.01). Macrophages, DCs, and alveolar epithelial cells were the main sources of CCL18. There was a direct correlation between the levels of tissue CCL18 and the number of lymphocytes in the bronchoalveolar lavage fluids. High levels of CCL18 were detected in the subacute rather than the chronic phase of HP. These findings suggest a role for CCL18 in the pathogenesis of HP.

摘要

过敏性肺炎(HP)是一种以T淋巴细胞积聚为特征的肺部炎症性疾病。然而,这一过程中涉及的机制仍不明确。我们检测了10例HP患者、9例特发性肺纤维化(IPF)患者和20例健康者肺组织中树突状细胞(DC)衍生的CC趋化因子1(CK1)/CCL18的表达,CCL18是一种可能参与幼稚T细胞募集的趋化因子。通过实时定量PCR检测CCL18,并通过原位杂交和免疫组织化学在肺组织中定位。与IPF患者的肺组织(2,085±393 vs. 1,023±110;P<0.05)和对照组(2,085±393 vs. 467±94;P<0.01)相比,HP患者受累肺组织中CCL18表达显著增加。巨噬细胞、DC和肺泡上皮细胞是CCL18的主要来源。组织CCL18水平与支气管肺泡灌洗液中淋巴细胞数量之间存在直接相关性。在HP的亚急性期而非慢性期检测到高水平的CCL18。这些发现提示CCL18在HP发病机制中起作用。

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