| Autor: |
Manuel G Feria, Cecilia Chang, Eduardo Ticona, Anissa Moussa, Bin Zhang, Isabel Ballena, Ruben Azañero, Cesar Ticona, Carlo N De Cecco, Carl J Fichtenbaum, Robert E O’Donnell, Alberto La Rosa, Jorge Sanchez, Sandra Andorf, Laura Atehortua, Jonathan D Katz, Claire A Chougnet, George S Deepe, Moises A Huaman |
| Rok vydání: |
2022 |
| Předmět: |
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| Zdroj: |
Open Forum Infectious Diseases. 9 |
| ISSN: |
2328-8957 |
| Popis: |
BackgroundLatent tuberculosis infection (LTBI) has been associated with increased cardiovascular risk. We investigated the activation and pro-inflammatory profile of monocytes in individuals with LTBI and their association with coronary artery disease (CAD).MethodsIndividuals 40–70 years old in Lima, Peru, underwent QuantiFERON-TB testing to define LTBI, completed a coronary computed tomography angiography to evaluate CAD, and provided blood for monocyte profiling using flow cytometry. Cells were stimulated with lipopolysaccharide to assess interleukin-6 (IL-6) and tumor necrosis factor (TNF)–α responses.ResultsThe clinical characteristics of the LTBI (n = 28) and non-LTBI (n = 41) groups were similar. All monocyte subsets from LTBI individuals exhibited higher mean fluorescence intensity (MFI) of CX3CR1 and CD36 compared with non-LTBI individuals. LTBI individuals had an increased proportion of nonclassical monocytes expressing IL-6 (44.9 vs 26.9; P = .014), TNF-α (62.3 vs 35.1; P = .014), and TNF-α+IL-6+ (43.2 vs 36.6; P = .042). Among LTBI individuals, CAD was associated with lower CX3CR1 MFI on classical monocytes and lower CD36 MFI across all monocyte subsets. In multivariable analyses, lower CD36 MFI on total monocytes (b = −0.17; P = .002) and all subsets remained independently associated with CAD in LTBI.ConclusionsIndividuals with LTBI have distinct monocyte alterations suggestive of an exacerbated inflammatory response and tissue migration. Whether these alterations contribute to cardiovascular disease pathogenesis warrants further investigation. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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