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IL13 Promoter (-1055) Polymorphism Associated with Leukocyte Mitochondria DNA Copy Number in Chronic Obstructive
Shih-Feng Liu1,2,3, Hui-Chuan Chang1, Yu-Ping Chang2,3
1Department of Respiratory Therapy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
Abstract:
IL13 polymorphism is associated with chronic obstructive pulmonary disease (COPD). Patients with COPD have smaller numbers of mitochondria deoxyribonucleic acid copies (mtDNA-CN) than people without COPD do. However, whether IL13 polymorphism affects the mutation and recombination of mitochondria remains unclear. Data for patients with COPD and non-COPD were collected from Kaohsiung Chang Gung Memorial Hospital to enable a comparison of their leukocyte mtDNA-CN and the association of this information with IL-13 promoter (−1055) polymorphism. This study included 99 patients with COPD and 117 individuals without COPD. The non-COPD individuals included 77 healthy individuals that never smoked and 40 healthy smokers. The patients with COPD exhibited significantly lower mtDNA-CN than non-COPD did (250.34 vs. 440.03; p < 0.001); mtDNA-CN was particularly pronounced in individuals with the IL13 CC and CT genotypes compared with individuals with the TT genotype. When only individuals without COPD were considered and when all participants were considered, the differences in the mtDNA-CNs in individuals with the CC and CT genotypes were more significant than those in individuals with the TT genotype (448.4 and 533.6 vs. 282.8; p < 0.05 in non-COPD group); (368.8 and 362.6 vs. 249.6, p < 0.05 in all participants). The increase mtDNA-CN in the CC and CT genotypes was also more than that in the TT genotype in COPD patients, but showed no significance (260.1 and 230.5 vs. 149.9; p = 0.343). The finding shows that COPD is a mitochondria regulatory disorder and IL-13 promoter (−1055) polymorphism is associated with leukocyte mtDNA-CN. Developing COPD control methods based on mitochondrial regulation will be possible.
Insights
Interleukin-13 (IL13) gene variations impact mitochondrial DNA copy number (mtDNA-CN) in chronic obstructive pulmonary disease (COPD) patients. This suggests IL13 polymorphism influences COPD development through mitochondrial regulation.
Area of Science:
- Genetics and Molecular Biology
- Pulmonology
- Mitochondrial Biology
Background:
- Chronic obstructive pulmonary disease (COPD) is linked to Interleukin-13 (IL13) genetic variations.
- Patients with COPD exhibit reduced mitochondrial DNA copy number (mtDNA-CN) compared to healthy individuals.
- The specific impact of IL13 polymorphism on mitochondrial DNA mutations and recombination in COPD remains largely unexplored.
Purpose of the Study:
- To investigate the association between IL-13 promoter (−1055) polymorphism and leukocyte mtDNA-CN in individuals with and without COPD.
- To determine if IL13 polymorphism influences mtDNA-CN levels in the context of COPD.
- To explore the potential of mitochondrial regulation as a therapeutic target for COPD.
Main Methods:
- A comparative study involving 99 COPD patients and 117 non-COPD individuals (including healthy non-smokers and smokers).
- Measurement of leukocyte mtDNA-CN in all participants.
- Genotyping for IL-13 promoter (−1055) polymorphism (TT, CT, CC genotypes).
Main Results:
- COPD patients showed significantly lower leukocyte mtDNA-CN (250.34) compared to non-COPD individuals (440.03; p < 0.001).
- Individuals with IL13 CC and CT genotypes had significantly higher mtDNA-CN than those with the TT genotype, particularly in the non-COPD and overall participant groups (p < 0.05).
- While higher mtDNA-CN was observed in CC and CT genotypes within the COPD group, this difference was not statistically significant (p = 0.343).
Conclusions:
- COPD may be characterized as a disorder involving mitochondrial regulation.
- IL-13 promoter (−1055) polymorphism is significantly associated with leukocyte mtDNA-CN.
- Findings support the potential for developing COPD management strategies targeting mitochondrial regulation.
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