Shorter telomeres in non-smoking patients with airflow limitation

Córdoba-Lanús, Elizabeth; Cabrera-López, Carlos; Cazorla-Rivero, Sara; Rodríguez-Pérez, María Cristo; Aguirre‐Jaime, Armando; Celli, Bartolomé R.; Casanova, Ciro

doi:10.1016/j.rmed.2018.04.002

Cited by 7 publications

(7 citation statements)

References 44 publications

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“…A somewhat surprising finding was that the multivariable analysis showed that cumulative smoking exposure in ever smokers did not affect the relationship between TL and lung function at any age. Yet, this observation is in keeping with the results of a meta-analysis of 18 longitudinal cohorts by Bateson et al indicating that smoking does not accelerate leucocyte telomere attrition (48), and with those of Cordoba et al showing that telomere shortening is associated with the airflow limitation independently of the smoking status (16). Importantly, it does not detract from the firmly established view that smoking is a key environmental risk factor for COPD (3); it only indicates that smoking per se does not influence the relationship between TL and lung function.…”

Section: Interpretation Of Novel Findingssupporting

confidence: 89%

“…Telomerase mutations and telomere attrition are described in alveolar type II and endothelial cells in patients with severe emphysema (34)(35)(36) and in mice models of smoking exposure (37). Other studies reported shortened telomeres (15) in old patients with COPD vs. controls (12,13,15,16) and a modest association between TL and FEV 1 % ref. (13), albeit the latter was not reproduced in other investigations (13-15, 38, 39).…”

Section: Previous Studiesmentioning

confidence: 99%

“…Further, their correlation can provide insights into the regulation of the ageing process (11). Previous studies have shown that both telomere length (TL) (5,(12)(13)(14)(15)(16) and mitochondrial DNA copy number (mtDNA-CN, as a surrogate marker of mitochondrial dysfunction) (17) in the circulating leukocytes are reduced in the old patients with COPD, but they have not been investigated in young patients with COPD so far. Likewise, their relationship with the smoking history of the patient, the severity of airflow limitation, or degree of emphysema present have not been studied in this setting either.…”

Section: Introductionmentioning

confidence: 99%

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Telomere Length but Not Mitochondrial DNA Copy Number Is Altered in Both Young and Old COPD

et al. 2021

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Accelerated ageing is implicated in the pathogenesis of respiratory diseases as chronic obstructive pulmonary disease (COPD), but recent evidence indicates that the COPD can have roots early in life. Here we hypothesise that the accelerated ageing markers might have a role in the pathobiology of young COPD. The objective of this study was to compare two hallmarks of ageing, telomere length (TL), and mitochondrial DNA copy number (mtDNA-CN, as a surrogate marker of mitochondrial dysfunction) in young (≤ 50 years) and old (>50 years) smokers, with and without COPD. Both, TL and mtDNA-CN were measured in whole blood DNA by quantitative PCR [qPCR] in: (1) young ever smokers with (n = 81) or without (n = 166) COPD; and (2) old ever smokers with (n = 159) or without (n = 29) COPD. A multivariable linear regression was used to assess the association of TL and mtDNA-CN with lung function. We observed that in the entire study population, TL and mtDNA-CN decreased with age, and the former but not the latter related to FEV1/FVC (%), FEV1 (% ref.), and DLCO (% ref.). The short telomeres were found both in the young and old patients with severe COPD (FEV1 <50% ref.). In addition, we found that TL and mtDNA-CN were significantly correlated, but their relationship was positive in younger while negative in the older patients with COPD, suggesting a mitochondrial dysfunction. We conclude that TL, but not mtDNA-CN, is associated with the lung function impairment. Both young and old patients with severe COPD have evidence of accelerated ageing (shorter TL) but differ in the direction of the correlation between TL and mtDNA-CN in relation to age.

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Section: Interpretation Of Novel Findingssupporting

confidence: 89%

Section: Previous Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Telomere Length but Not Mitochondrial DNA Copy Number Is Altered in Both Young and Old COPD

et al. 2021

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“…The authors refer to a separate study reporting that COPD patients have significantly shorter blood leucocyte telomeres than healthy controls (12) and Córdoba-Lanús et al suggest that airflow limitation is associated with shortened telomere lengths (13). However, Doherty et al did not report airflow and other lung function parameters, presence or absence of COPD, or other comorbidities associated with altered telomere length in their cohort.…”

Section: Confounding Effectsmentioning

confidence: 96%

Subtype variation and actionability of telomere length abnormality in lung cancer

Goh¹,

Yang²,

Bowman³

et al. 2018

Transl. Lung Cancer Res.

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“…In most somatic cells, TL shortens with each cellular division until a critical point, beyond which cells enter a stage of replicative senescence. In adult populations without HIV, shorter leukocyte TL has been associated with reduced lung function [ 11 , 12 ], airflow limitation in nonsmokers [ 13 ], chronic obstructive pulmonary disease (COPD) [ 14 ], and asthma [ 15 ]. In the context of HIV, the infection itself is associated with shorter leukocyte TL in adults without and with respiratory diseases [ 16–19 ], and in the latter, shorter TL was also measured in small airway epithelial cells [ 20 ].…”

mentioning

confidence: 99%

Shorter Granulocyte Telomeres Among Children and Adolescents With Perinatally Acquired Human Immunodeficiency Virus Infection and Chronic Lung Disease in Zimbabwe

Ajaykumar

Wong

Yindom

et al. 2020

Clinical Infectious Diseases

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Background Chronic lung disease (CLD) has been reported among African children with perinatally-acquired HIV infection (C-PHIV), despite combination antiretroviral therapy (cART). In adults, shorter telomere length (TL) has been reported in association with both CLD and HIV. As little is known in children, our objective was to compare TL in HIV+ (cART-naïve or treated) and HIV-negative children with and without CLD. Methods Participants included Zimbabwean C-PHIV, aged 6-16, who were either newly diagnosed and cART-naïve, or on cART for >6 months, and HIV-negative controls of similar age and sex. Packed blood cell (granulocyte) TL from 621 children were compared cross-sectionally between groups. For a subset of newly diagnosed C-PHIV, changes in TL following cART initiation was evaluated. Results C-PHIV had shorter granulocyte TL compared to uninfected peers, regardless of cART. Among 255 C-PHIV without CLD, TL was shorter in cART-naïve participants. In multivariable analyses adjusted for age, sex, CLD, and HIV/cART status, shorter TL was independently associated with older age, being HIV+, and having reduced forced vital capacity (FVC). Lastly, cART initiation increased TL. Conclusions In this cohort, C-PHIV and those with reduced FVC have shorter granulocyte TL, possibly the result of increased immune activation and cellular turnover due to long-standing HIV infection with delayed cART initiation.

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Shorter telomeres in non-smoking patients with airflow limitation

Abstract: Telomere shortening is associated with airflow limitation independent of smoking status. Weather premature ageing or biologically determined shorter telomeres are responsible for this finding remain to be determined.

Cited by 7 publications

References 44 publications

Telomere Length but Not Mitochondrial DNA Copy Number Is Altered in Both Young and Old COPD

Telomere Length but Not Mitochondrial DNA Copy Number Is Altered in Both Young and Old COPD

Subtype variation and actionability of telomere length abnormality in lung cancer

Shorter Granulocyte Telomeres Among Children and Adolescents With Perinatally Acquired Human Immunodeficiency Virus Infection and Chronic Lung Disease in Zimbabwe

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