Genetic variants in ADAM33 are associated with airway inflammation and lung function in COPD

Wang, Xinyan; Wan, Li; Huang, Kun; Kang, Xiaowen; Li, Zhaoguo; Yang, Chengcheng; Wu, Xiaomei; Chen, Lina

doi:10.1186/1471-2466-14-173

Cited by 13 publications

(13 citation statements)

References 46 publications

(52 reference statements)

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“…The current results were in accordance with Wang et al, 12 they confirmed that T1 and T2 ADAM33 SNPs were significantly associated with decreased FEV 1 and FEV 1 /FVC. ADAM33 is selectively expressed in mesenchymal cells.…”

Section: Discussionsupporting

confidence: 93%

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Association of ADAM33 gene polymorphism and arginase activity with susceptibility to ventilatory impairment in wood dust-exposed workers

et al. 2016

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ADAM33 represents an important gene of susceptibility for lung function impairment. This work aimed to evaluate the association between genetic polymorphism of ADAM33 at four single nucleotide polymorphisms (T1, T2, S1, and Q1) and arginase activity with respiratory functions impairment in wood workers. The study was done to compare ventilatory functions and arginase activity of 82 wood workers and 81 controls. Genotyping was determined by using the polymerase chain restriction fragment length polymorphism method. Forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), and peak expiratory flow rate (PEF) of the workers were significantly reduced compared with the controls. T1 single nucleotide polymorphism (SNP) was associated with obvious decline in the FEV1, FVC, and PEF in wood workers, while T2 SNP was associated with decline in FEV1 and PEF. A significant increase in arginase activity was found in T2 and S1 SNPs of the exposed workers. Increase in duration of exposure was correlated with the decline in ventilatory functions. This inverse correlation was significant for pulmonary function indices in AA and GG genotypes of T1 and T2, respectively. Moreover, significance was detected for FVC and FEV1 in AA and GA genotypes of S1 and Q1. A positive correlation between arginase activity and duration of exposure was found to be significant in GG genotype of S1 SNP. An association between ADAM33 gene polymorphism and impaired lung functions was detected in wood dust-exposed workers. Arginase activity may play an associated important role in increasing this impairment in wood workers.

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Section: Discussionsupporting

confidence: 93%

“…11 Additional studies have demonstrated that single nucleotide polymorphisms (SNPs) within ADAM33 were associated with accelerated decline of lung function in the general population and in asthmatic patients. 12 Arginase exists as two distinct isoenzymes, arginase I and II, which are encoded by different genes.…”

Section: Introductionmentioning

confidence: 99%

Association of ADAM33 gene polymorphism and arginase activity with susceptibility to ventilatory impairment in wood dust-exposed workers

et al. 2016

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“…Метаболически устойчивый аналог пурина ИНО-2002 оказывал противовоспалительное действие при остром респираторном дистресссиндроме [42]. Мышей заражали интратрахеально ЛПС (50 мкг), затем через 1-5 часов вводили внутрибрюшинно INO-2002.…”

Section: рис 1 динамика уровней Tnfα и Il-10 при исследовании эффекunclassified

Modern immunotherapy for chronic obstructive pulmonary disease

Ishchenko¹,

Novikov²,

Сукало³

2019

Immunopathol Allergol Infectol

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Введение. Всемирная организация здравоохранения включила ХОБЛ в группу заболеваний, имеющих приоритетное значение для общественного здравоохранения, для которых фармацевтическое лечение является неадекватным. Цель работы: анализ различных направлений современной иммунотерапии ХОБЛ и сопоставление их с результатами собственных исследований. Материал и методы. Обзор литературы проведён в системах PubMed, Cochrane, Medline, Google Scholar, library. Анализ клинико-иммунологической эффективности иммуномодуляторов лейаргунала, иммугенина и иммунофизиокоррекции, проведен на основе данных 1,2 фазы клинических испытаний и клинического исследования трех методов физиотерапии (УЗ на область тимуса, КВЧ и лазеротеротерапия). Результаты. Международный союз базовой и клинической фармакологии (IUPHAR) и Британское фармакологическое общество (BPS) относят ХОБЛ к иммунным заболеваниям. В базе данных GtoPdb включено 42 иммунных лиганда, ассоциированных с ХОБЛ. Основные направления связаны с антивоспалительным механизмом: ингибиторы протеинкиназы MAPp38; хемокиновых рецепторов CXCR2, CXCR1, CCR2; блокаторы ММР-9 и ММР-12; антагониста рецептора лейкотриена B4 (BLT1), прямые или опосредованные ингибиторы PI3K; ингибиторы pan-JAK; блокаторы нейтрофильной эластазы и др. Опубликованы противоречивые результаты исследований, посвященных эффективности моноклональных антител против интерлейкинов 1β, 5, 8, 13 и TNFα. Иммунокоррекция иммугенином нормализовала как клеточный, так и гуморальный иммунитет, что клинически привело к снижению количества обострений и удлинению промежутка времени между обострениями. Применение лейаргунала удлиняло ремиссию (р=0,021) и сокращало число рецидивов (р=0,042), что позволило предотвратить Summary Introduction. The World Health Organization has included COPD in the group of diseases that are a priority for public health, for which pharmaceutical treatment is inadequate. Objective. Aim was analysis of various ways of modern COPD immunotherapy and comparing them with the results of their own research. Material and methods. The literature review was conducted in PubMed, Cochrane, Medline, Google Scholar, Elibrary. The analysis of the clinical and immunological efficacy of immunomodulators leyargunal, immunogenin and immunophysiocorrection was carried out on the basis of data from phase 1,2 clinical trials and blind randomized controlled clinical prospective comparative study of three physiotherapy methods (ultrasound on the thymus area, EHF and laser-therapy). Results. The International Union of Basic and Clinical Pharmacology (IUPHAR) and the British Pharmacological Society (BPS) classify COPD as an immune disease. The GtoPdb database includes 42 immune ligands associated with COPD. The main directions are related to the antiinflammatory mechanism: MAPp38 inhibitors; chemokine receptors CXCR2, CXCR1, CCR2; MMP-9 and MMP-12 blockers; leukotriene B4 receptor antagonist (BLT1), direct or indirect inhibitors of PI3K; pan-JAK inhibitors; neutrophil elastase blockers, etc. The controversial results of studies on the e...

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“…9 Multiple studies have shown that ADAM family members, including ADAM8, ADAM17, ADAM33 might participate in the pathogenesis of COPD. [10][11][12][13] ADAM9 is normally expressed in epithelial cells, inflammatory cells, and smooth muscle cells in human lung tissues. 14 A murine study using an ADAM9 knockout mice model showed alleviated airspace enlargement in response to cigarette smoking exposure, which indicated its importance in emphysema.…”

Section: Introductionmentioning

confidence: 99%

“… 9 Multiple studies have shown that ADAM family members, including ADAM8, ADAM17, ADAM33 might participate in the pathogenesis of COPD. 10–13 …”

Section: Introductionmentioning

confidence: 99%

<p>Relationship Between Proteinase with a Disintegrin and a Metalloproteinase Domain-9 (ADAM9), Inflammation, Airway Remodeling, and Emphysema in COPD Patients</p>

Cui

Xie

et al. 2020

COPD

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Background and Objective The link between ADAM9 and airway remodeling and emphysema severity in COPD patients has not been elucidated. Here, we investigated the relationship between ADAM9 levels in sputum and airway epithelium and the clinical characteristics of COPD patients. Methods A sputum cohort and a lung tissue cohort were included in the study. Pulmonary function and computed tomography data were analyzed in COPD patients, non-COPD smokers, and non-smokers. Soluble ADAM9 and interleukin 8 (IL-8) levels in sputum supernatants as well as surface ADAM9 expression in airway epithelium were detected. Emphysema scores were calculated by the percentage of low attenuation area (%LAA-950), and airway remodeling was measured via airway thickening and loss of airway counts. Results Both soluble ADAM9 levels in sputum and relative surface ADAM9 expression in airway epithelium were increased in COPD patients. Sputum ADAM9 levels were negatively correlated with forced expiratory volume in 1 s of predicted (FEV1% of predicted) and positively correlated with sputum IL-8 levels, but not with CT measured emphysema nor airway remodeling. The ADAM9 expression in airway epithelia was positively correlated with %LAA-950 and airway wall thickening parameters (wall area percentage, WA%; the square root of the wall area in a standard airway with a 10 mm internal perimeter, Pi-10), while negatively correlated with airway counts derived from the 4th to 9th bronchial generations. Conclusion Airway ADAM9 levels in sputum and airway epithelium were both elevated in COPD patients compared to non-COPD controls. Sputum ADAM9 seemed to be associated with inflammatory responses in COPD, while epithelial ADAM9 was more correlated with emphysema and airway remodeling.

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Genetic variants in ADAM33 are associated with airway inflammation and lung function in COPD

Cited by 13 publications

References 46 publications

Association of ADAM33 gene polymorphism and arginase activity with susceptibility to ventilatory impairment in wood dust-exposed workers

Association of ADAM33 gene polymorphism and arginase activity with susceptibility to ventilatory impairment in wood dust-exposed workers

Modern immunotherapy for chronic obstructive pulmonary disease

<p>Relationship Between Proteinase with a Disintegrin and a Metalloproteinase Domain-9 (ADAM9), Inflammation, Airway Remodeling, and Emphysema in COPD Patients</p>

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