Corry-Anke Brandsma

Introduction Coronavirus disease 2019 (COVID-19), caused by SARS coronavirus 2 (SARS-CoV-2), has disproportionately affected individuals with chronic obstructive pulmonary disease (COPD) [1-6]. COPD is a common lung disease characterized by chronic respiratory symptoms caused by airway (chronic bronchitis) and alveolar (emphysema) changes in the lung, resulting in irreversible airflow limitation [7].

Abstract Background: Lung fibroblasts from Severe Early-Onset (SEO-)COPD patients exhibit increased cellular senescence with higher levels of senescence-associated secretory phenotype (SASP) protein secretion. Yet, the impact of senescent fibroblasts, and their SASP, on surrounding fibroblasts in SEO-COPD lungs remains unclear. Aim: To identify the effect of the SASP secreted by senescent SEO-COPD-derived fibroblasts on surrounding lung fibroblasts.

Abstract Cellular senescence has been recognized to play a role in COPD pathophysiology. Non-aerosolized E-liquid treatment of a lung fibroblast foetal cell line resulted in cellular senescence induction, but this has not been assessed using E-vapour exposure and using primary lung fibroblasts. Therefore, we investigated whether E-vapour exposure induces cellular senescence in primary human lung fibroblasts and whether this affects their tissue repair function.