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.

免疫衰老是在整个个体生命中发生的免疫系统变化。这个过程的主要特征是复制性衰老，通过端粒缩短来评估。有几个因素与端粒缩短有关，例如吸烟。在这项研究中，我们评估了吸烟和慢性阻塞性肺病 (COPD) 对细胞因子、端粒长度和端粒酶活性的影响。

血液样本采集自 60 岁以上的受试者：健康（从不吸烟）、吸烟者（吸烟 30 年以上）和慢性阻塞性肺病（戒烟者 ≥15 年）。包括一个年轻组作为对照。培养 PBMC 以使用 RT-PCR 和细胞因子分泌流式细胞术评估端粒酶活性。CD4+ 和 CD8+ 纯化的淋巴细胞用于使用 FlowFISH 评估端粒长度。

我们观察到 COPD 患者的端粒缩短速度加快。矛盾的是，没有肺损伤的吸烟者显示出保留的端粒长度，这表明吸烟可能会影响调节机制，例如端粒酶。与 COPD 和健康组相比，端粒酶活性在 COPD 中的活性降低，而吸烟者的活性则在增加。

细胞外环境反映了这种不平衡，吸烟者的抗炎特征表明，而慢性阻塞性肺病则表现出易发炎的特征。进一步关注端粒维持的研究可能会揭示长期吸烟与癌症相关的机制。