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<p>Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality globally. COPD, within its context of disease etiology, is characterized by chronic inflammation of the lungs. It is distinguished by the aberrant production of oxidants, inflammatory cytokines, dysregulated immune cell activity, and remodeling of the airways. In this study, we analyzed the polymorphic association of antioxidants (<i>GSTM1/T1</i>) and inflammation-related genes (<i>CXCL8, IL-33,</i> and <i>IL-6</i>) with COPD. A case–control study was conducted with 227 subjects (116 healthy controls and 111 COPD cases). <i>GSTM1/T1&#xa0;genes were amplified by multiplex PCR‚</i> and inflammatory genes (<i>CXCL8</i>, <i>IL-33</i>, and <i>IL-6</i>) were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR–RFLP) method. <i>GSTM1</i>/<i>T1</i> gene deletion rates in the COPD group were significantly higher than those in the control group (<i>GSTM1</i>: OR = 11.85, CI = 4.033–34.79, <i>P</i> &lt; 0.0001; <i>GSTT1</i>: OR = 2.303, CI = 1.206–4.399, <i>P</i> = 0.0113). In addition, our research revealed a significant association between the combined <i>GSTM1/T1</i> null genotype and increased susceptibility to COPD (OR = 18.66, CI = 2.345–148.5, <i>P</i> = 0.0003). A significantly increased frequency of the “CC” genotype of the <i>CXCL8</i> (rs2227532) gene variant (OR = 7.50, CI = 2.429–23.16, <i>P</i> &lt; 0.0001) was observed in COPD patients compared to the control group. However, there was no significant association of the <i>IL-33</i> (rs7044343) polymorphism between healthy controls and COPD patients. The <i>IL-6</i> (rs2069860) gene variant was found to be monomorphic. As a result of the investigation, it was concluded that individuals with the null genotype of <i>GSTM1/T1</i> combined and the presence of the CXCL8 (rs2227532) gene variant have a higher likelihood of developing COPD.</p>

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Association of polymorphisms of antioxidants (GSTM1/T1) and inflammation-related genes (CXCL8, IL-33, and IL-6) with chronic obstructive pulmonary disease (COPD)

  • 期刊论文

  • 发表日期：

    2025年11月6日

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  • Osaid Masood,
  • Saurabh Kumar,
  • Surya Kant,
  • Monisha Banerjee

摘要

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality globally. COPD, within its context of disease etiology, is characterized by chronic inflammation of the lungs. It is distinguished by the aberrant production of oxidants, inflammatory cytokines, dysregulated immune cell activity, and remodeling of the airways. In this study, we analyzed the polymorphic association of antioxidants (GSTM1/T1) and inflammation-related genes (CXCL8, IL-33, and IL-6) with COPD. A case–control study was conducted with 227 subjects (116 healthy controls and 111 COPD cases). GSTM1/T1 genes were amplified by multiplex PCR‚ and inflammatory genes (CXCL8, IL-33, and IL-6) were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR–RFLP) method. GSTM1/T1 gene deletion rates in the COPD group were significantly higher than those in the control group (GSTM1: OR = 11.85, CI = 4.033–34.79, P < 0.0001; GSTT1: OR = 2.303, CI = 1.206–4.399, P = 0.0113). In addition, our research revealed a significant association between the combined GSTM1/T1 null genotype and increased susceptibility to COPD (OR = 18.66, CI = 2.345–148.5, P = 0.0003). A significantly increased frequency of the “CC” genotype of the CXCL8 (rs2227532) gene variant (OR = 7.50, CI = 2.429–23.16, P < 0.0001) was observed in COPD patients compared to the control group. However, there was no significant association of the IL-33 (rs7044343) polymorphism between healthy controls and COPD patients. The IL-6 (rs2069860) gene variant was found to be monomorphic. As a result of the investigation, it was concluded that individuals with the null genotype of GSTM1/T1 combined and the presence of the CXCL8 (rs2227532) gene variant have a higher likelihood of developing COPD.