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非吸烟酒精性肝硬化患者肺泡巨噬细胞单因子分泌及mRNA表达受损。

Impaired secretion and mRNA expression of monokines by alveolar macrophages from nonsmoking patients with alcoholic liver cirrhosis.

作者信息

Gosset P, Wallaert B, Canva-Delcambre V, Colombel J F, Tonnel A B

机构信息

INSERM U416, Institut Pasteur, Lille, France.

出版信息

J Infect Dis. 1995 Mar;171(3):743-6. doi: 10.1093/infdis/171.3.743.

Abstract

Alveolar macrophages (AM) exposed to microorganisms secrete cytokines that are important to lung defense. Since alcoholic liver cirrhosis (ALC) patients are susceptible to lung infections, the ability of AM in such patients to produce the cytokines tumor necrosis factor-alpha, interleukin (IL)-1 beta, and IL-6 was evaluated by mRNA expression and protein secretion. Adherent AM from ALC and alcoholic patients and controls were cultured with and without lipopolysaccharide (LPS): Mean cytokine levels in ALC and alcoholic subjects were not significantly different than in controls. However, LPS-stimulated AM from 13 of 29 ALC patients exhibited a reduced ability, compared with that from controls, to secrete the cytokines (P < .05 for all 3). Specific mRNA expression was also impaired in the 13 patients, and their liver diseases were more severe than those of other patients. Impaired cytokine production by AM in ALC patients with severe cirrhosis may account for their increased susceptibility to lung infections.

摘要

暴露于微生物的肺泡巨噬细胞(AM)会分泌对肺部防御很重要的细胞因子。由于酒精性肝硬化(ALC)患者易患肺部感染,因此通过mRNA表达和蛋白质分泌评估了此类患者的AM产生细胞因子肿瘤坏死因子-α、白细胞介素(IL)-1β和IL-6的能力。将来自ALC患者、酗酒患者和对照组的贴壁AM在有和没有脂多糖(LPS)的情况下进行培养:ALC患者和酗酒受试者的细胞因子平均水平与对照组相比无显著差异。然而,与对照组相比,29例ALC患者中有13例的LPS刺激的AM分泌细胞因子的能力降低(所有3种细胞因子P均<0.05)。这13例患者的特异性mRNA表达也受损,且他们的肝脏疾病比其他患者更严重。严重肝硬化的ALC患者中AM的细胞因子产生受损可能是他们对肺部感染易感性增加的原因。

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