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[肺泡巨噬细胞对鸟分枝杆菌复合群的细胞内杀伤机制]

[Intracellular killing mechanisms of alveolar macrophages against Mycobacterium avium complex].

作者信息

Suga M, Doi T, Akaike T, Ando M

机构信息

Internal Medicine of Kumamoto Rosai Hospital, Japan.

出版信息

Kekkaku. 1992 Jan;67(1):55-62.

PMID:1371815
Abstract

To clarify the intracellular killing mechanisms of alveolar macrophages against Mycobacterium avium complex, effects of cytokines on O2- and NO2- production from normal and BCG-induced alveolar macrophages were studied. Intracellular growth of M. avium complex was inhibited in the alveolar macrophages stimulated by TNF, but not IFN. Enhancement of O2- production by normal alveolar macrophages stimulated by cytokines, was associated with the inhibition of intracellular growth of M. avium complex. However, when NO2- production by the alveolar macrophages was enhanced by the stimulating of IFN or IFN+TNF, in the presence L-arginine in the culture medium, their defense activity against M. avium complex decreased.

摘要

为阐明肺泡巨噬细胞对鸟分枝杆菌复合群的细胞内杀伤机制,研究了细胞因子对正常及卡介苗诱导的肺泡巨噬细胞产生超氧阴离子(O2-)和二氧化氮(NO2-)的影响。肿瘤坏死因子(TNF)刺激的肺泡巨噬细胞可抑制鸟分枝杆菌复合群的细胞内生长,但干扰素(IFN)则无此作用。细胞因子刺激正常肺泡巨噬细胞使其超氧阴离子产生增加,这与鸟分枝杆菌复合群细胞内生长受抑制相关。然而,当培养基中存在L-精氨酸时,干扰素或干扰素+肿瘤坏死因子刺激肺泡巨噬细胞使其二氧化氮产生增加,它们对鸟分枝杆菌复合群的防御活性却降低了。

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