Bonecini-Almeida M da G, Werneck-Barroso E, Carvalho P B, de Moura C P, Andrade E F, Hafner A, Carvalho C E, Ho J L, Kritski A L, Morgado M G
AIDS and Molecular Immunology Laboratory, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, RJ, Brazil. galmeida@gene. dbbm.fiocruz.br
Cell Immunol. 1998 Dec 15;190(2):112-20. doi: 10.1006/cimm.1998.1399.
We compared the peripheral and pulmonary response to assess the phagocytic activity of monocytes/macrophages and neutrophils and the lymphoproliferative response (LPR) against Mycobacterium tuberculosis antigens from 21 AIDS patients, presenting at diagnosis with active pulmonary tuberculosis (TB), other non-TB pulmonary infection, or no pulmonary infection, as well as patients with active pulmonary TB and healthy control subjects. Alveolar lymphocyte analysis demonstrated that AIDS/TB patients had more markedly reduced percentages of CD4(+) lymphocytes than AIDS/TB patients and an increase in the percentage of CD8(+) lymphocytes, probably reflecting the impairment of CD4(+) T lymphocytes in peripheral blood at the lungs. Moreover, alveolar lymphocytes from AIDS/TB patients demonstrated a two- to fourfold decrease in LPR against M. tuberculosis antigens. Interestingly, it was observed an enhanced migration of natural killer cells to the lungs in all patients group. The phagocytic activity in alveolar macrophages and neutrophils showed that AIDS/TB patients had a twofold decreased capacity to ingest inert particles compared with AIDS patients. Comparing the alveolar and peripheral lymphocyte number and functional activity to M. tuberculosis-antigens it was possible to demonstrate that in both sites these cells had similar profile. However, the innate immune response in lungs showed a reduced activation in the presence of HIV infection, regarding the M. tuberculosis coinfection. These findings suggest that the advanced impairment of CD4(+) T lymphocyte in HIV-1 infection may lead to a deactivation of alveolar macrophages, enhancing bacilli burden and HIV replication in the lungs and furthering dissemination.
我们比较了外周和肺部反应，以评估21例艾滋病患者单核细胞/巨噬细胞和中性粒细胞的吞噬活性以及针对结核分枝杆菌抗原的淋巴细胞增殖反应（LPR）。这些艾滋病患者在诊断时患有活动性肺结核（TB）、其他非结核肺部感染或无肺部感染，同时还包括活动性肺结核患者和健康对照者。肺泡淋巴细胞分析表明，艾滋病/肺结核患者的CD4(+)淋巴细胞百分比比艾滋病/非肺结核患者明显降低，而CD8(+)淋巴细胞百分比增加，这可能反映了肺部外周血中CD4(+) T淋巴细胞的损伤。此外，艾滋病/肺结核患者的肺泡淋巴细胞对结核分枝杆菌抗原的LPR降低了两到四倍。有趣的是，在所有患者组中均观察到自然杀伤细胞向肺部的迁移增强。肺泡巨噬细胞和中性粒细胞中的吞噬活性表明，与艾滋病患者相比，艾滋病/肺结核患者摄取惰性颗粒的能力降低了两倍。比较肺泡和外周淋巴细胞数量以及对结核分枝杆菌抗原的功能活性，可以证明在这两个部位这些细胞具有相似的特征。然而，就结核分枝杆菌合并感染而言，在存在HIV感染的情况下，肺部的先天免疫反应显示出激活减少。这些发现表明，HIV-1感染中CD4(+) T淋巴细胞的严重损伤可能导致肺泡巨噬细胞失活，增加肺部的杆菌负荷和HIV复制，并促进传播。
