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Corleis, Björn; Cho, Josalyn L; Gates, Samantha J; Linder, Alice H; Dickey, Amy; Lisanti-Park, Antonella C; Schiff, Abigail E; Ghebremichael, Musie; Kohli, Puja; Winkler, Tilo; Harris, R Scott; Medoff, Benjamin D; Kwon, Douglas S
American journal of respiratory cell and molecular biology, 11/2021, Letnik: 65, Številka: 5Journal Article
Smoking and human immunodeficiency virus 1 (HIV-1) infection are risk factors for chronic obstructive pulmonary disease (COPD), which is among the most common comorbid conditions in people living with HIV-1. HIV-1 infection leads to persistent expansion of CD8 T cells, and CD8 T cell-mediated inflammation has been implicated in COPD pathogenesis. In this study, we investigated the effects of HIV-1 infection and smoking on T-cell dynamics in patients at risk of COPD. BAL fluid, endobronchial brushings, and blood from HIV-1 infected and uninfected nonsmokers and smokers were analyzed by flow cytometry, and lungs were imaged by computed tomography. Chemokines were measured in BAL fluid, and CD8 T-cell chemotaxis in the presence of cigarette smoke extract was assessed . HIV-1 infection increased CD8 T cells in the BAL fluid, but this increase was abrogated by smoking. Smokers had reduced BAL fluid concentrations of the T cell-recruiting chemokines CXCL10 and CCL5, and cigarette smoke extract inhibited CXCL10 and CCL5 production by macrophages and CD8 T-cell transmigration . In contrast to the T cells in BAL fluid, CD8 T cells in endobronchial brushings were increased in HIV-1-infected smokers, which was driven by an accumulation of effector memory T cells in the airway mucosa and an increase in tissue-resident memory T cells. Mucosal CD8 T-cell numbers inversely correlated with lung aeration, suggesting an association with inflammation and remodeling. HIV-1 infection and smoking lead to retention of CD8 T cells within the airway mucosa.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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