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肿瘤坏死因子α单克隆抗体预防小鼠肺炎链球菌诱导的肺实变

[Streptococcus pneumoniae-induced pulmonary consolidation prevented with tumor necrosis factor alpha monoclonal antibody in mouse].

作者信息

Cui X, Zhang R, Fu W

机构信息

Laboratory of Pulmonary Disease, Union Hospital, Tongji Medical University, Wuhan.

出版信息

Zhonghua Yi Xue Za Zhi. 1995 Jan;75(1):19-21, 61.

PMID:7600313
Abstract

Streptococcus pneumoniae stimulate mouse peritoneal macrophages to release tumor necrosis factor alpha (TNF alpha) in vitro. When penicillin was added to lysate bacterium, TNF alpha release was accelerated. 150 Kunming mice were infected with streptococcus pnumoniae through inspiration. Dynamic changes of TNF alpha concentration in serum and bronchoalveolar lavage fluid were detected; pulmonary pathological changes were also observed. It was found that TNF alpha monoclonal antibody significantly attenuates TNF alpha activity in serum and bronchoalveolar lavage fluid, white blood cell chemotaxis, emigation, and infiltration were inhibited. We conclude that streptococcus pneumoniae infection stimulates TNF alpha release, and TNF alpha is probably the major mediator that causes tissue damage during streptococcus pneumoniae infection. As penicillin accelerates TNFa release, single therapy of penicillin may worse tissue damage.

摘要

肺炎链球菌在体外刺激小鼠腹腔巨噬细胞释放肿瘤坏死因子α(TNFα)。当将青霉素添加到裂解细菌中时,TNFα的释放加速。150只昆明小鼠通过吸入感染肺炎链球菌。检测血清和支气管肺泡灌洗液中TNFα浓度的动态变化;同时观察肺部病理变化。发现TNFα单克隆抗体显著减弱血清和支气管肺泡灌洗液中TNFα的活性,白细胞趋化性、游出及浸润均受到抑制。我们得出结论,肺炎链球菌感染刺激TNFα释放,并且TNFα可能是肺炎链球菌感染期间导致组织损伤的主要介质。由于青霉素加速TNFα释放,单独使用青霉素治疗可能会加重组织损伤。

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