Human Immunodeficiency Virus, Smoking, and Chronic Obstructive Pulmonary Disease: A Case of T Cells Stuck in the Wrong Place?
| Autor: | Robert M Tighe, Sweta M Patel |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Adult
Male Pulmonary and Respiratory Medicine Receptors CXCR3 Receptors CCR5 T-Lymphocytes Clinical Biochemistry Human immunodeficiency virus (HIV) MEDLINE Pulmonary disease HIV Infections Respiratory Mucosa CD8-Positive T-Lymphocytes medicine.disease_cause Pulmonary Disease Chronic Obstructive Risk Factors medicine Humans Chemokine CCL5 Molecular Biology Original Research Mucous Membrane business.industry Chemotaxis Smoking Editorials virus diseases HIV Cell Biology Middle Aged Viral Load respiratory system respiratory tract diseases Chemokine CXCL10 Immunology HIV-1 Female Tomography X-Ray Computed business Bronchoalveolar Lavage Fluid |
| Zdroj: | Am J Respir Cell Mol Biol American Journal of Respiratory Cell and Molecular Biology |
| ISSN: | 1535-4989 1044-1549 |
| Popis: | 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 in vitro. 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 vitro. 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. |
| Databáze: | OpenAIRE |
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