ArticleAmerican journal of respiratory cell and molecular biology2008
IL10 polymorphisms are associated with airflow obstruction in severe alpha1-antitrypsin deficiency.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Pooled it
- Review
- Article
- A polygenic risk score and age of diagnosis of COPD.The European respiratory journal · 2022Article
- Polymorphisms in HumanGenes · 2022Article
- Recent advancements in understanding the genetic involvement of alpha-1 antitrypsin deficiency associated lung disease: a look at future precision medicine approaches.Expert review of respiratory medicine · 2022Review
- Alpha-1 antitrypsin deficiency in the elderly: a case report.Journal of medical case reports · 2021Article
- Why is Disease Penetration So Variable? Role of Genetic Modifiers of Lung Function in Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Leveraging Population Genomics for Individualized Correction of the Hallmarks of Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Vitamin D (1,25(OH)The Journal of steroid biochemistry and molecular biology · 2019Article
- Relationship of systemic IL-10 levels with proinflammatory cytokine responsiveness and lung function in agriculture workers.Respiratory research · 2018Article
- Alpha-1 antitrypsin deficiency: outstanding questions and future directions.Orphanet journal of rare diseases · 2018Review
- Glutathione-S-transferase P1 may predispose children to a decline in pulmonary function after stem cell transplant.Pediatric pulmonology · 2017Article
- Chronic obstructive pulmonary disease candidate gene prioritization based on metabolic networks and functional information.PloS one · 2017Article
- Mapping genetic determinants of host susceptibility to Pseudomonas aeruginosa lung infection in mice.BMC genomics · 2016Article
- Clinical Trial Design for Alpha-1 Antitrypsin Deficiency: A Model for Rare Diseases.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2015Article
- Clarification of the risk of chronic obstructive pulmonary disease in α1-antitrypsin deficiency PiMZ heterozygotes.American journal of respiratory and critical care medicine · 2014Article
- Article
- Nitric oxide synthase polymorphisms, gene expression and lung function in chronic obstructive pulmonary disease.BMC pulmonary medicine · 2013Article
- Human "orchestrator" CD11b(+) B1 cells spontaneously secrete interleukin-10 and regulate T-cell activity.Molecular medicine (Cambridge, Mass.) · 2012Article
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Authors and funding
13 authors at 11 institutions in 2 countries.
Funding
Abstract
Severe alpha(1)-antitrypsin (AAT) deficiency is a proven genetic risk factor for chronic obstructive pulmonary disease (COPD), especially in individuals who smoke. There is marked variability in the development of lung disease in individuals homozygous (PI ZZ) for this autosomal recessive condition, suggesting that modifier genes could be important. We hypothesized that genetic determinants of obstructive lung disease may be modifiers of airflow obstruction in individuals with severe AAT deficiency. To identify modifier genes, we performed family-based association analyses for 10 genes previously associated with asthma and/or COPD, including IL10, TNF, GSTP1, NOS1, NOS3, SERPINA3, SERPINE2, SFTPB, TGFB1, and EPHX1. All analyses were performed in a cohort of 378 PI ZZ individuals from 167 families. Quantitative spirometric phenotypes included forced expiratory volume in one second (FEV(1)) and the ratio of FEV(1)/forced vital capacity (FVC). A qualitative phenotype of moderate-to-severe COPD was defined for individuals with FEV(1) </= 50 percent predicted. Six of 11 single-nucleotide polymorphisms (SNPs) in IL10 (P = 0.0005-0.05) and 3 of 5 SNPs in TNF (P = 0.01-0.05) were associated with FEV(1) and/or FEV(1)/FVC. IL10 SNPs also demonstrated association with the qualitative COPD phenotype. When phenotypes of individuals with a physician's diagnosis of asthma were excluded, IL10 SNPs remained significantly associated, suggesting that the association with airflow obstruction was independent of an association with asthma. Haplotype analysis of IL10 SNPs suggested the strongest association with IL10 promoter SNPs. IL10 is likely an important modifier gene for the development of COPD in individuals with severe AAT deficiency.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.