Immunology in COPD and the use of combustible cigarettes and heated tobacco products

Abstract

Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases, characterised by high morbidity and mortality. COPD is characterised by a progressive decline of lung function caused by chronic inflammatory reactions in the lung tissue due to continual exposure to harmful molecules by inhalation. As prevention plays a very important role in COPD, quitting smoking is the most important factor in reducing the decline in lung function. Unfortunately, many people are unable to break their nicotine addiction. This paper summarises current knowledge about combustible cigarettes (CSs) and alternative tobacco products such as heated tobacco products (HTPs) in COPD. The paper focuses on the immunological aspects of COPD and the influence of tobacco products on lung tissue immunology. There are differences in research results between HTPs and CSs in favour of HTPs. More long-term studies are needed to look at the effects of HTPs, especially in COPD. However, there is no doubt that it would be best for patients to give up their nicotine addiction completely.

Exploring the Common Genetic Underpinnings of Chronic Pulmonary Disease and Esophageal Carcinoma Susceptibility

“…Our research findings suggest the potential existence of shared genetic mechanisms between esophageal cancer and pulmonary diseases. Enrichment analysis indicates that these pleiotropic loci involve various biological pathways, such as behavioral responses to nicotine 51 - 54 , adipocyte differentiation 55 , 56 , nuclear speckles 57 , 58 , responses to fatty acids 59 , 60 , and granulocyte differentiation 61 , among others. These pathways are associated with processes like smoking, inflammation, and immune function, contributing to an explanation of the interconnections between diseases.…”

Neutrophil extracellular traps and their implications in airway inflammatory diseases

“…COPD is a common and treatable inflammatory disease characterized by progressive airflow limitation and tissue destruction (112,113). Stimuli such as cigarette smoke, environmental pollutants, bacteria, viruses, and oxidative stress induce the secretion of chemokines and inflammatory mediators by lung epithelial cells and macrophages, which in turn attract neutrophils and monocytes from the circulation to infiltrate the lung tissue, causing sustained inflammation (114)(115)(116)(117).…”