title: Functional activity of alveolar and peripheral cells in patients with human acquired immunodeficiency syndrome and pulmonary tuberculosis.
abstract: 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.
authors.affiliation: AIDS and Molecular Immunology Laboratory, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, RJ, Brazil. galmeida@gene. dbbm.fiocruz.br
authors.forename: M da G
authors.initials: Mda G
authors.lastname: Bonecini-Almeida
authors.forename: E
authors.initials: E
authors.lastname: Werneck-Barroso
authors.forename: P B
authors.initials: PB
authors.lastname: Carvalho
authors.forename: C P
authors.initials: CP
authors.lastname: de Moura
authors.forename: E F
authors.initials: EF
authors.lastname: Andrade
authors.forename: A
authors.initials: A
authors.lastname: Hafner
authors.forename: C E
authors.initials: CE
authors.lastname: Carvalho
authors.forename: J L
authors.initials: JL
authors.lastname: Ho
authors.forename: A L
authors.initials: AL
authors.lastname: Kritski
authors.forename: M G
authors.initials: MG
authors.lastname: Morgado
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000097:blood / Q000276:immunology*; D000328:Adult; D002455:Cell Division; D005260:Female; D015497:HIV-1; D006801:Humans; D008214:Lymphocytes / Q000276:immunology*; D016676:Macrophages, Alveolar / Q000276:immunology*; D008297:Male; D009504:Neutrophils / Q000276:immunology; D010586:Phagocytes / Q000276:immunology; D011650:Pulmonary Alveoli / Q000166:cytology / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D014373:Tuberculin / Q000276:immunology; D014397:Tuberculosis, Pulmonary / Q000097:blood / Q000150:complications / Q000276:immunology*
chemical_list: D014373:Tuberculin