de Noronha Almério L L, Báfica André, Nogueira Lucas, Barral Aldina, Barral-Netto Manoel
Centro de Pesquisas Goncalo Moniz, Fiocruz, Bahia, Brazil; Faculdade de Medicina da Bahia, UFBA, Salvador, Bahia, Brazil.
Pathol Res Pract. 2008;204(3):155-61. doi: 10.1016/j.prp.2007.10.008. Epub 2007 Dec 21.
Tuberculosis/HIV-1 co-infection is responsible for thousands of deaths each year, and previous studies have reported that co-infected individuals display major morphological alterations in tissue granulomas. The purpose of this study was to evaluate immunohistopathological characteristics in lung tissues from pulmonary TB/HIV-1-co-infected individuals. Following autopsy, tuberculosis-positive HIV-1-negative cases displayed granulomas with normal architecture, mainly composed of a mononuclear infiltrate with typical epithelioid, as well as giant cells, and exhibiting caseous necrosis. In contrast, lesions from the TB/HIV-1-co-infected group showed extensive necrosis, poorly formed granulomas, and a marked presence of polymorphonuclear cells. More importantly, TNF staining was greatly reduced in the TB/HIV-1-co-infected individuals. Our data suggest that HIV-1 infection alters the organization of pulmonary granulomas by modulating TNF and, possibly, cell trafficking, leading to an impaired anti-tuberculosis response.
结核病与HIV-1合并感染每年导致数千人死亡，先前的研究报道，合并感染个体的组织肉芽肿出现了主要的形态学改变。本研究的目的是评估肺结核合并HIV-1感染个体肺组织的免疫组化病理特征。尸检后，结核阳性HIV-1阴性病例的肉芽肿结构正常，主要由单核浸润组成，伴有典型上皮样细胞以及巨细胞，并出现干酪样坏死。相比之下，结核与HIV-1合并感染组的病变显示广泛坏死、肉芽肿形成不良以及多形核细胞明显增多。更重要的是，结核与HIV-1合并感染个体的TNF染色显著减少。我们的数据表明，HIV-1感染通过调节TNF以及可能的细胞转运改变肺肉芽肿的组织结构，导致抗结核反应受损。
