Habit smoke influences both innate and adaptive immune responses, although its effect on innate responses is lost with smoking cessation, but on the other hand, changes in adaptive responses persist even years after quitting tobacco, according to a new study published in the journal ”Nature‘.
In this study, current smokers experienced a stronger inflammatory response after exposure to certain bacteria, which quickly disappeared when they quit smoking. Against, The effects of tobacco on T-cell responses persist years after people quit smoking.
People vary greatly in their immune responses because Age, gender and genetic factors play an important role. Within this internal variability, there are other external factors that can change the defense. However, the variables that mediate such differences in cytokine secretion (a critical component of the host response to immunological challenges) remain poorly understood.
To this end, the researchers analyzed 136 variables and identified smoking, latent cytomegalovirus (CMV) infection and body mass index as the main factors influencing variability in cytokine response, with effects comparable in magnitude to age, sex and genetics.
Thus they discovered that Smoking is one of the external factors that most influences immune responses. both innate and adaptive. In particular, its effects on innate responses are rapidly lost after smoking cessation and are specifically associated with plasma CEACAM6 levels, whereas its effects on adaptive responses persist long after people quit smoking and are associated with epigenetic memory.
The results identify three new variables associated with variability in cytokine secretion and reveal the role of smoking in the short- and long-term regulation of immune responses. These findings have potential clinical implications for the risk of developing infections, cancer, or autoimmune diseases.
To come to this conclusion, experts collected 1,000 human samples Milieu Intérieur cohorts. Donors were required to have no history or evidence of serious, chronic or recurrent medical conditions, neurological or psychiatric disorders, alcohol abuse, recent drug use, recent vaccine administration, and recent use of immunomodulatory agents.
To identify novel environmental factors associated with variability in response to immune stimulation, researchers focused on cytokine protein secretion as a phenotype of the immune response, which included concentrations of 13 cytokines relevant to disease and medicine.
Stimulants are divided into four categories: microbial (Bacillus Calmette-Guerin (BCG), E. coli, lipopolysaccharide (LPS) and Candida albicans (C. albicans) and viral (influenza and polyinosinic acid-polycytidylic acid (poly I:C)), agents that are predominantly recognized by receptors on innate immune cells; T-cell activators (staphylococcal enterotoxin B superantigen (SEB) and anti-CD3 and anti-CD28 antibodies (anti-CD3 + CD28)) that induce adaptive immune responses and cytokines (TNF, IL-1 and IFN).
To assess the biological impact of smoking on cytokine secretion, they plotted effect sizes for smoking variables from linear models. So they noticed that current smoking affects immune responses as tobacco is associated with stronger induction of the cytokine CXCL5 after E. coli stimulation and stronger induction of IL-2 and IL-13 after SEB stimulation. Variables related to smoking (number of years of smoking, number of years since last smoking, and total number of cigarettes smoked) showed a consistent association.
In addition, he emphasizes that, unlike current smokers, former smokers do not show a significant increase in CXCL5 secretion after innate immune stimulation, while they exhibited increased secretion of IL-2 and IL-13 after adaptive immune stimulation compared to individuals who had never smoked.
In summary, smoking, latent CMV infection, and body mass index, in addition to age, sex, genetic variations, DNA methylation levels, and immune cell subsets, have been shown to be variables more associated with changes in cytokine secretion following immunological challenge. .
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