About this Research Topic
Tobacco smoking is a worldwide epidemic and is one of the most critical risk factors associated with the development of cardiovascular and respiratory diseases, besides being considered a leading cause of cancer death. Many countries have reported increasing consumption rates, particularly among adolescents and women, and at an early age onset. Most smokers have a nicotine addiction, a complex and multifactorial disease affecting the central nervous system. Moreover, epidemiological studies have reported that environmental factors also play a role in disease development.
In addition to the neuronal nicotinic acetylcholine receptors (nAChRs) subunit genes, the internationally validated loci for smoking quantity and nicotine addiction/dependence (the CHRNA5-CHRNA3-CHRNB4 and the CHRNB3-CHRNA6 clusters), the genes encoding the receptors involved in the dopaminergic and serotonergic pathways (DRD4 and HTR2A) and those encoding the main enzyme responsible for nicotine metabolism (CYP2A6) have been identified in the mechanisms of nicotine addiction.
However, the studies focused on gene-regulated inflammatory factors acting in concert with those in nicotine addiction are scanty. Most of these have been reported in respiratory diseases secondary to tobacco smoking, such as chronic obstructive pulmonary disease (COPD), lung cancer, interstitial lung diseases, asthma, cardiovascular disease, and COVID-19, mainly suggesting a role in the disease severity or worse prognosis. Studies evaluating the effect of smoking on immunological diseases by considering genetic information employing a gene-environment interaction approach are required. In addition, most of the reports have been done in Caucasian and Asian populations, and studies in admixed/mestizo populations are needed to validate initial findings in immunogenetics-related factors.
Given the need to develop additional knowledge in this field, in this research topic, we aim to address the role of genetic/genomic immunological factors contributing to clinical manifestations in tobacco smoking/nicotine addiction and respiratory and systemic diseases to identify target markers in therapeutics and rehabilitation in affected subjects.
We welcome original research and review papers contributing to novel information on the relationship between immunogenetics and clinical and translational research in tobacco smoking/nicotine addiction and gene-environment interaction studies.
Potential topics include, but are not limited to, the following:
1. The genetic susceptibility factors concerning immune-related molecules and their association to tobacco smoking and diseases or phenotypes related.
2. Epigenetic changes (including methylation, but not only) in genes encoding inflammatory and immunological molecules in nicotine addiction/tobacco smoking and related diseases.
3. Variability among populations in immunogenetic factors in respiratory and systemic diseases and its involvement in disease severity.
4. Coding and non-coding RNAs (including microRNAs) and their involvement in tobacco smoking and related diseases.
5. Polymorphisms associated with response to smoking cessation therapies and related quantitative traits.
6. Studies on the genetic heterogeneity of nicotine addiction on a gender basis.
7. The influence of immunogenetics on host-microbiome interactions in nicotine addiction and disease and phenotypes related.
8. Gene-environment interaction studies evaluating the effect of cigarette smoking, air pollution, or other environmental pollutants on lung function and inflammatory diseases and their quantitative phenotypic traits.
In addition to the neuronal nicotinic acetylcholine receptors (nAChRs) subunit genes, the internationally validated loci for smoking quantity and nicotine addiction/dependence (the CHRNA5-CHRNA3-CHRNB4 and the CHRNB3-CHRNA6 clusters), the genes encoding the receptors involved in the dopaminergic and serotonergic pathways (DRD4 and HTR2A) and those encoding the main enzyme responsible for nicotine metabolism (CYP2A6) have been identified in the mechanisms of nicotine addiction.
However, the studies focused on gene-regulated inflammatory factors acting in concert with those in nicotine addiction are scanty. Most of these have been reported in respiratory diseases secondary to tobacco smoking, such as chronic obstructive pulmonary disease (COPD), lung cancer, interstitial lung diseases, asthma, cardiovascular disease, and COVID-19, mainly suggesting a role in the disease severity or worse prognosis. Studies evaluating the effect of smoking on immunological diseases by considering genetic information employing a gene-environment interaction approach are required. In addition, most of the reports have been done in Caucasian and Asian populations, and studies in admixed/mestizo populations are needed to validate initial findings in immunogenetics-related factors.
Given the need to develop additional knowledge in this field, in this research topic, we aim to address the role of genetic/genomic immunological factors contributing to clinical manifestations in tobacco smoking/nicotine addiction and respiratory and systemic diseases to identify target markers in therapeutics and rehabilitation in affected subjects.
We welcome original research and review papers contributing to novel information on the relationship between immunogenetics and clinical and translational research in tobacco smoking/nicotine addiction and gene-environment interaction studies.
Potential topics include, but are not limited to, the following:
1. The genetic susceptibility factors concerning immune-related molecules and their association to tobacco smoking and diseases or phenotypes related.
2. Epigenetic changes (including methylation, but not only) in genes encoding inflammatory and immunological molecules in nicotine addiction/tobacco smoking and related diseases.
3. Variability among populations in immunogenetic factors in respiratory and systemic diseases and its involvement in disease severity.
4. Coding and non-coding RNAs (including microRNAs) and their involvement in tobacco smoking and related diseases.
5. Polymorphisms associated with response to smoking cessation therapies and related quantitative traits.
6. Studies on the genetic heterogeneity of nicotine addiction on a gender basis.
7. The influence of immunogenetics on host-microbiome interactions in nicotine addiction and disease and phenotypes related.
8. Gene-environment interaction studies evaluating the effect of cigarette smoking, air pollution, or other environmental pollutants on lung function and inflammatory diseases and their quantitative phenotypic traits.
Keywords: Polymorphisms, HLA, CYP2A6, Inflammation, Cytokine, Interleukin, Nicotine addiction, Tobacco Smoking, Lung diseases, Cardiovascular diseases, COVID-19, gene-environment
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