Preferential recruitment of phagocytes into the lung of patients with advanced acquired immunodeficiency syndrome and tuberculosis

Citation
E. Werneck-barroso et al., Preferential recruitment of phagocytes into the lung of patients with advanced acquired immunodeficiency syndrome and tuberculosis, RESP MED, 94(1), 2000, pp. 64-70
Citations number
36
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
RESPIRATORY MEDICINE
ISSN journal
09546111 → ACNP
Volume
94
Issue
1
Year of publication
2000
Pages
64 - 70
Database
ISI
SICI code
0954-6111(200001)94:1<64:PROPIT>2.0.ZU;2-T
Abstract
Limited data are available on the cellular and immunocytological characteri stics of bronchoalveolar lavage (BAL) fluid in individuals infected with th e human immunodeficiency virus (HIV) and pulmonary tuberculosis (TB). The i mmune host response against tuberculosis in early HIV-infection may differ from that in later stages of HIV disease, as is strongly suggested by diffe rent clinical and radiographic patterns. We studied the cellular elements i n the lungs of 15 HIV-infected patients with advanced immunosuppression and pulmonary tuberculosis (TB/AIDS). The findings were compared with data fro m four other groups: 1) 15 HIV-seronegative patients with pulmonary TB; 2) 12 HIV-seropositive TB patients without previous AIDS-defining illnesses an d with CD4+ > 200 cells mm(-3); 3) five AIDS patients without pulmonary les ions; and 4) five healthy controls, BAL fluid and differential cell counts? as well as lymphocyte subsets, were determined. Despite a low CD4/CD8 rati o, the TB/AIDS group had a higher absolute number of CD8+ lymphocytes in th e BAL fluid than the other groups. Alveolar macrophages and neutrophils wer e significantly increased in TB/AIDS patients compared to control groups. T he number of eosinophils was increased in TB/HIV- patients but not in TB/AI DS patients. We conclude that tuberculosis in Late stage HIV-infected patie nts has a distinct inflammatory cell profile, suggesting an enhanced compen satory mechanism that amplifies the unspecific inflammatory reaction.