Journal of Clinical and Cellular Immunology
Open Access

Impact of Cigarette Smoking on Immune System

Young Xian^{* *}Correspondence: Young Xian, Department of Immunology, Xiangya Hospital, Central South University, China, Email:

Author info »

Description

Cigarette smoking is related to a variety of diseases and poses a severe threat to the current healthcare system around the world. Smoking has an impact on both innate and adaptive immunity, and it regulates immunity in two ways: by exacerbating pathogenic immunological responses and attenuating defensive immunity. T helper cells (Th1/Th2/Th17), CD4⁺ CD25⁺ regulatory T cells, CD8⁺ T cells, B cells, and memory T/B lymphocytes are among the adaptive immune cells impacted by smoking, whereas DCs, macrophages, and NK cells are among the innate immune cells damaged by smoking. Complex roles of cigarette smoke have resulted in numerous diseases, including cardiovascular, respiratory and autoimmune diseases, allergies, cancers and transplant rejection etc. Although previous have discussed the effects of smoking on numerous diseases and regional immunity associated with specific diseases, a full and up-to-date evaluation of the effects of smoking on general immunity and, in particular, main components of immune cells is rarely observed. The goal of this paper is to provide a thorough and objective overview of the effects of smoking on important components of both innate and adaptive immune cells, as well as a summary of the cellular and molecular mechanisms behind cigarette smoking's immune system impacts. Cigarette smoking affects molecular pathways such as NFB, MAP kinases, and histone modification.

Cigarette smoking is widespread in many countries, with an estimated 1/3 of the adult population smoking tobacco. Tobacco smoke contains a variety of hazardous substances, including carbon monoxide, nicotine, nitrogen oxides, and cadmium, among others. Tobacco smoke exposure is linked to the development of brain, respiratory, cardiovascular, and infectious disorders, as well as malignancies, and is a leading cause of premature mortality globally. In the meanwhile, smoking has been linked to the generation of a variety of immunological and inflammatory mediators, including pro-inflammatory and antiinflammatory cytokines. Many recent studies have shown that cigarette smoking has far-reaching impacts on chronic inflammation and autoimmune at the systemic level, including Rheumatoid Arthritis (RA), psoriasis, Chronic Obstructive Pulmonary Disease (COPD), and Systemic Lupus Erythematous (SLE). Although prior reviews have described the effects of cigarette smoking on numerous diseases and local immunity linked with a specific disease, there has yet to be a thorough evaluation establishing the effects of cigarette smoking on important components of immune cells. Consumers previously discovered that smoking reduces the long-term survival of allografts generated by stimulatory blocking. The goal of this paper is to evaluate the dual impacts of smoking on key components of immune cells in both innate and adaptive immunity, as well as outline the molecular and cellular mechanisms behind these effects.

T lymphocytes

T lymphocytes (T cells) are a type of immune cell that plays a role in adaptive immunity. When naive T cells are activated and differentiated in response to antigen recognition, they produce effector T cells and, to a lesser extent, memory and regulatory T cells. These cells use their helper, effector, cytotoxic, and regulatory abilities in response to certain antigens. Previous research has demonstrated that cigarette smoking has a significant impact on T cells and their release of proinflammatory mediators.

T helper cells

Cigarette smoking has long been recognised as a primary cause of COPD, which is characterised by chronic airway restriction. T cells were found in 40 non-smokers, 40 smokers with normal pulmonary function, and 38 COPD patients' Broncho Alveolar Lavage (BAL) fluid and central blood. They observed that smoking groups had a larger percentage of CD8⁺ BAL cells than non-smoking groups, whereas smokers had a lower frequency of CD4⁺ T cells in both BAL and blood than non-smokers. When compared to healthy non-smokers, the equilibrium of circulating T helper cells was altered in chronic COPD patients. T cell components were also altered by Second Hand Smoking (SHS). Passive smoking was positively connected with the proportion of naive CD3⁺ T cells, according to analyses of blood cotinine, a nicotine metabolite, and T-cell subpopulations from nonsmokers. In humans, active smoking increases the percentage of CD8⁺ T cells while decreasing the percentage of CD4⁺ T cells, whereas passive smoking increases the percentage of human CD3⁺ T cells.