Functional activity of alveolar and peripheral cells in patients with human acquired immunodeficiency syndrome and pulmonary tuberculosis

Citation
Mdg. Bonecini-almeida et al., Functional activity of alveolar and peripheral cells in patients with human acquired immunodeficiency syndrome and pulmonary tuberculosis, CELL IMMUN, 190(2), 1998, pp. 112-120
Citations number
39
Categorie Soggetti
Immunology
Journal title
CELLULAR IMMUNOLOGY
ISSN journal
00088749 → ACNP
Volume
190
Issue
2
Year of publication
1998
Pages
112 - 120
Database
ISI
SICI code
0008-8749(199812)190:2<112:FAOAAP>2.0.ZU;2-N
Abstract
We compared the peripheral and pulmonary response to assess the phagocytic activity of monocytes/macrophages and neutrophils and the lymphoproliferati ve 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 pat ients with active pulmonary TB and healthy control subjects. Alveolar lymph ocyte 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 o f 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 gr oup. The phagocytic activity in alveolar macrophages and neutrophils showed that AIDS/TB patients had a twofold decreased capacity to ingest inert par ticles compared with AIDS patients. Comparing the alveolar and peripheral l ymphocyte 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 HN infection, regarding the M. tuberculosis coinfection. These findings suggest that the advanced impairment of CD4+ T lymphocyte i n HIV-1 infection may lead to a deactivation of alveolar macrophages, enhan cing bacilli burden and HIV replication in the lungs and furthering dissemi nation. (C) 1998 Academic Press.