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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Long-term tobacco exposure and immunosenescence: Paradoxical effects on T-cells telomere length and telomerase activity

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Fernandes, Juliana Ruiz [1] ; Pinto, Thalyta Nery Carvalho [1] ; Piemonte, Lucas Lopes [2] ; Arruda, Lia Barbara [3] ; da Silva, Cibele Cristine Berto Marques [4] ; Carvalho, Celso R. F. [4] ; Pinto, Regina Maria Carvalho [5] ; Duarte, Alberto J. S. [1] ; Benard, Gil [1]
Total Authors: 9
[1] Univ Sao Paulo, Sch Med, Lab Dermatol & Immunodeficiencies LIM56, Av Dr Arnaldo 455, Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Med, Permanent Educ Sch, Av Dr Ovidio Pires Campo 471, Sao Paulo - Brazil
[3] UCL, Royal Free Hosp Campus, Ctr Clin Microbiol, Div Infect & Immun, London - England
[4] Univ Sao Paulo, Sch Med, Dept Phys Therapy, R Dr Ovidio Pires Campos 255, Sao Paulo - Brazil
[5] Univ Sao Paulo, Sch Med, Heart Inst InCor, Pulm Dept, Av Dr Eneas Carvalho Aguiar 44, Sao Paulo - Brazil
Total Affiliations: 5
Document type: Journal article
Web of Science Citations: 0

Immunosenescence are alterations on immune system that occurs throughout an individual life. The main characteristic of this process is replicative senescence, evaluated by telomere shortening. Several factors implicate on telomere shortening, such as smoking. In this study, we evaluated the influence of smoking and Chronic Obstructive Pulmonary Disease (COPD) on cytokines, telomere length and telomerase activity. Blood samples were collected from subjects aged over 60 years old: Healthy (never smokers), Smokers (smoking for over 30 years) and COPDs (ex-smokers for >= 15 years). A young group was included as control. PBMCs were cultured for assessment of telomerase activity using RT-PCR, and cytokines secretion flow cytometry. CD4+ and CD8+ purified lymphocytes were used to assess telomere length using FlowFISH. We observed that COPD patients have accelerated telomere shortening. Paradoxically, smokers without lung damage showed preserved telomere length, suggesting that tobacco smoking may affect regulatory mechanisms, such as telomerase. Telomerase activity showed diminished activity in COPDs, while Smokers showed increased activity compared to COPDs and Healthy groups. Extracellular environment reflected this unbalance, indicated by an anti-inflammatory profile in Smokers, while COPDs showed an inflammatory prone profile. Further studies focusing on telomeric maintenance may unveil mechanisms that are associated with cancer under long-term smoking. (AU)

FAPESP's process: 18/06063-8 - Immunosenescence on Chronic Obstructive Pulmonary Disease
Grantee:Gil Benard
Support type: Regular Research Grants