Abstract
IL-17A is an important pro-inflammatory cytokine involved in the inflammatory response in chronic obstructive pulmonary disease (COPD). To evaluate the role played by single nucleotide polymorphisms of IL17A and protein levels in susceptibility to COPD, 1,807 subjects were included in a case-control study; 436 had COPD related to tobacco smoking (COPD-S) and 190 had COPD related to biomass burning (COPD-BB). Six hundred fifty-seven smokers without COPD (SWOC) and 183 biomass burning-exposed subjects (BBES) served as the respective control groups. The CC genotype and C allele of rs8193036 were associated with COPD (COPD-S vs. SWOC: p < 0.05; OR = 3.01, and OR = 1.28, respectively), as well as a recessive model (p < 0.01; OR = 2.91). Significant differences in serum levels were identified between COPD-S vs. SWOC, COPD-S vs. COPD-BB, and SWOC vs. BBES (p < 0.01). By comparing genotypes in the COPD-BB group TT vs. CC and TC vs. CC (p < 0.05), we found lower levels for the CC genotype. Logistic regression analysis by co-variables was performed, keeping the associations between COPD-S vs. SWOC with both polymorphisms evaluated (p < 0.05), as well as in COPD-BB vs. BBES but with a reduced risk of exacerbation (p < 0.05). In conclusion, polymorphisms in IL17A are associated with COPD. Serum levels of IL-17A were higher in smokers with and without COPD.
Highlights
According to the Global Initiative for Chronic Obstructive Lung Diseases (GOLD) guidelines, chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable disease that is distinguished by persistent respiratory symptoms and airflow limitation, which is due to airway abnormalities usually caused by significant exposure to noxious particles or gases, with tobacco smoking and biomass burning indoors being the major risk factors[1]
Age and sex were significantly different between COPD related to tobacco smoking (COPD-S) and COPD related to biomass burning (COPD-BB) patients vs. smokers without COPD (SWOC) and burningexposed subjects (BBES) groups, respectively (COPD groups are older than the controls, and the COPD-S group is predominantly men, p < 0.01)
Our results have a classical behavior, determining that COPD related to smoking is more prevalent in male and older people and that COPD related to biomass burning is more prevalent in older women
Summary
According to the Global Initiative for Chronic Obstructive Lung Diseases (GOLD) guidelines, chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable disease that is distinguished by persistent respiratory symptoms and airflow limitation, which is due to airway abnormalities usually caused by significant exposure to noxious particles or gases, with tobacco smoking and biomass burning indoors being the major risk factors[1]. Despite being one of the most prevalent diseases in developed countries, the pathogenesis and factors involved in COPD have not been fully elucidated. Genetic associations have expanded our vision and have elucidated important mechanisms that participate in COPD. Since 2003, Agustí and coworkers[12] hypothesized that one of the possible pathogenic mechanisms in COPD is the existence of self-perpetuating inflammation, similar to other autoimmune diseases. This idea is supported by studies where autoantibodies have been identified in these patients, as well as previous reports that describe ongoing inflammation in COPD patients who do not currently smoke[13,14,15,16]. Th17 cells are increased in the peripheral blood in patients with COPD19
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