Elevated Levels of Interleukin-1β and Interleukin-10 Are Associated With Faster Lung Function Decline in People With Well-Treated Human Immunodeficiency Virus
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Elevated Levels of Interleukin-1β and Interleukin-10 Are Associated With Faster Lung Function Decline in People With Well-Treated Human Immunodeficiency Virus. / Thudium, Rebekka F; Arentoft, Nicoline S; Hoel, Hedda; Afzal, Shoaib; Von Stemann, Jakob H; Forman, Julie L; Wilcke, Jon T; Benfield, Thomas; Trøseid, Marius; Borges, Álvaro H; Ostrowski, Sisse R; Vestbo, Jørgen; Kunisaki, Ken M; Jensen, Jens-ulrik S; Nielsen, Susanne D.
I: The Journal of Infectious Diseases, Bind 228, Nr. 8, 2023, s. 1080–1088.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Elevated Levels of Interleukin-1β and Interleukin-10 Are Associated With Faster Lung Function Decline in People With Well-Treated Human Immunodeficiency Virus
AU - Thudium, Rebekka F
AU - Arentoft, Nicoline S
AU - Hoel, Hedda
AU - Afzal, Shoaib
AU - Von Stemann, Jakob H
AU - Forman, Julie L
AU - Wilcke, Jon T
AU - Benfield, Thomas
AU - Trøseid, Marius
AU - Borges, Álvaro H
AU - Ostrowski, Sisse R
AU - Vestbo, Jørgen
AU - Kunisaki, Ken M
AU - Jensen, Jens-ulrik S
AU - Nielsen, Susanne D
PY - 2023
Y1 - 2023
N2 - BackgroundPeople with human immunodeficiency virus (PWH) have an increased risk of chronic lung diseases and chronic inflammation. We aimed to investigate if inflammatory markers and monocyte activation are associated with faster lung function decline in PWH.MethodsWe included 655 PWH from the Copenhagen Comorbidity in HIV Infection (COCOMO) Study. Eligible participants were aged ≥25 years and had 2 spirometries separated by >2 years. Inflammatory markers (interleukin [IL]–1β, IL-2, IL-6, IL-10, tumor necrosis factor–α, and interferon-γ) were measured at baseline by Luminex, and soluble CD14 and soluble CD163 by enzyme-linked immunosorbent assay. Using linear mixed models, we investigated whether elevated cytokine levels were associated with faster lung function decline.ResultsThe majority of PWH were males (85.2%) with undetectable viral replication (95.3%). We found a faster decline in forced expiratory volume in 1 second (FEV1) in PWH with elevated IL-1β and IL-10, with an additional decline of 10.3 mL/year (95% confidence interval [CI], 2.1–18.6; P = .014) and 10.0 mL/year (95% CI, 1.8–18.2; P = .017), respectively. We found no interaction between smoking and IL-1β or IL-10 on FEV1 decline.ConclusionsElevated IL-1β and IL-10 were independently associated with faster lung function decline in PWH, suggesting that dysregulated systemic inflammation may play a role in the pathogenesis of chronic lung diseases.
AB - BackgroundPeople with human immunodeficiency virus (PWH) have an increased risk of chronic lung diseases and chronic inflammation. We aimed to investigate if inflammatory markers and monocyte activation are associated with faster lung function decline in PWH.MethodsWe included 655 PWH from the Copenhagen Comorbidity in HIV Infection (COCOMO) Study. Eligible participants were aged ≥25 years and had 2 spirometries separated by >2 years. Inflammatory markers (interleukin [IL]–1β, IL-2, IL-6, IL-10, tumor necrosis factor–α, and interferon-γ) were measured at baseline by Luminex, and soluble CD14 and soluble CD163 by enzyme-linked immunosorbent assay. Using linear mixed models, we investigated whether elevated cytokine levels were associated with faster lung function decline.ResultsThe majority of PWH were males (85.2%) with undetectable viral replication (95.3%). We found a faster decline in forced expiratory volume in 1 second (FEV1) in PWH with elevated IL-1β and IL-10, with an additional decline of 10.3 mL/year (95% confidence interval [CI], 2.1–18.6; P = .014) and 10.0 mL/year (95% CI, 1.8–18.2; P = .017), respectively. We found no interaction between smoking and IL-1β or IL-10 on FEV1 decline.ConclusionsElevated IL-1β and IL-10 were independently associated with faster lung function decline in PWH, suggesting that dysregulated systemic inflammation may play a role in the pathogenesis of chronic lung diseases.
U2 - 10.1093/infdis/jiad233
DO - 10.1093/infdis/jiad233
M3 - Journal article
C2 - 37366576
VL - 228
SP - 1080
EP - 1088
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
SN - 0022-1899
IS - 8
ER -
ID: 360769230