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为什么结核病会导致特定的炎症?

Why does tuberculosis lead to specific inflammation?

作者信息

Sugawara Isamu

机构信息

The Research Institute of Tuberculosis, Kiyose, Tokyo, Japan.

出版信息

Nihon Hansenbyo Gakkai Zasshi. 2009 Sep;78(3):263-9. doi: 10.5025/hansen.78.263.

DOI:10.5025/hansen.78.263
PMID:19803377
Abstract

When Mycobacterium tuberculosis infects humans, about 20% of those infected actually develop tuberculosis (TB). In Japan, the incidence of TB in 2008 was 24,760 cases (19.4/100,000 persons) and the rate has been decreasing gradually, but is still higher than in the USA, Holland, and Belgium, for example. Histologically, tuberculosis displays exudative inflammation, proliferative inflammation and productive inflammation depending on the time course. In productive inflammation, granulomatous lesions with necrotic centers are formed. The typical granulomas consist of epithelioid macrophages, Langhans' multinucleated giant cells, lymphocytes and fibroblasts, and the process of their formation involves many cytokines, chemokines and transcription factors. These findings have been derived primarily from animal experiments utilizing an airborne infection apparatus. The conditions for airborne infection have been described in detail elsewhere. This mini-review focuses on what has been found through animal experiments, and also indicates areas for which data are not currently available.

摘要

当结核分枝杆菌感染人类时,约20%的感染者会实际患上结核病(TB)。在日本,2008年结核病发病率为24,760例(每10万人中有19.4例),且发病率一直在逐渐下降,但仍高于美国、荷兰和比利时等国家。从组织学上看,结核病根据病程会表现出渗出性炎症、增生性炎症和增殖性炎症。在增殖性炎症中,会形成具有坏死中心的肉芽肿性病变。典型的肉芽肿由上皮样巨噬细胞、朗汉斯多核巨细胞、淋巴细胞和成纤维细胞组成,其形成过程涉及许多细胞因子、趋化因子和转录因子。这些发现主要来自利用空气传播感染装置进行的动物实验。空气传播感染的条件在其他地方已有详细描述。本综述聚焦于通过动物实验所发现的内容,同时也指出了目前尚无数据的领域。

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