Childhood asthma is a risk factor for the development of chronic obstructive pulmonary disease

McGeachie, Michael J.

doi:10.1097/aci.0000000000000348

Cited by 60 publications

(47 citation statements)

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“…There has been a growing interest in the risk of early life asthmatics for developing COPD, and thus ACO, in adulthood [ 15 ]. It has been proposed that in some childhood asthmatics, the risk for COPD is the result of the lungs never achieving their expected growth and development in early adulthood [ 11 , 12 , 16 , 20 , 52 , 53 ]. Normal decline in lung function can lead to COPD since expected maximal FEV 1 is never attained.…”

Section: Discussionmentioning

confidence: 99%

“…Childhood asthma is a genetically distinct asthma subtype, with estimated heritability of 68–92% [ 2 – 10 ]. Asthma is a known risk factor for development of reduced lung function and chronic obstructive pulmonary disease (COPD) in adults [ 11 – 14 ]. Asthmatics are often excluded from COPD studies, and thus information on the mechanism of disease and appropriate treatments for asthma-COPD overlap (ACO) remains limited [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Childhood asthma is associated with COPD and known asthma variants in COPDGene: a genome-wide association study

et al. 2018

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BackgroundChildhood asthma is strongly influenced by genetics and is a risk factor for reduced lung function and chronic obstructive pulmonary disease (COPD) in adults. This study investigates self-reported childhood asthma in adult smokers from the COPDGene Study. We hypothesize that childhood asthma is associated with decreased lung function, increased risk for COPD, and that a genome-wide association study (GWAS) will show association with established asthma variants.MethodsWe evaluated current and former smokers ages 45–80 of non-Hispanic white (NHW) or African American (AA) race. Childhood asthma was defined by self-report of asthma, diagnosed by a medical professional, with onset at < 16 years or during childhood. Subjects with a history of childhood asthma were compared to those who never had asthma based on lung function, development of COPD, and genetic variation. GWAS was performed in NHW and AA populations, and combined in meta-analysis. Two sets of established asthma SNPs from published literature were examined for association with childhood asthma.ResultsAmong 10,199 adult smokers, 730 (7%) reported childhood asthma and 7493 (73%) reported no history of asthma. Childhood asthmatics had reduced lung function and increased risk for COPD (OR 3.42, 95% CI 2.81–4.18). Genotype data was assessed for 8031 subjects. Among NHWs, 391(7%) had childhood asthma, and GWAS identified one genome-wide significant association in KIAA1958 (rs59289606, p = 4.82 × 10− 8). Among AAs, 339 (12%) had childhood asthma. No SNPs reached genome-wide significance in the AAs or in the meta-analysis combining NHW and AA subjects; however, potential regions of interest were identified. Established asthma SNPs were examined, seven from the NHGRI-EBI database and five with genome-wide significance in the largest pediatric asthma GWAS. Associations were found in the current childhood asthma GWAS with known asthma loci in IL1RL1, IL13, LINC01149, near GSDMB, and in the C11orf30-LRRC32 region (Bonferroni adjusted p < 0.05 for all comparisons).ConclusionsChildhood asthmatics are at increased risk for COPD. Defining asthma by self-report is valid in populations at risk for COPD, identifying subjects with clinical and genetic characteristics known to associate with childhood asthma. This has potential to improve clinical understanding of asthma-COPD overlap (ACO) and enhance future research into ACO-specific treatment regimens.Trial registrationClinicalTrials.gov, NCT00608764 (Active since January 28, 2008).Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0890-0) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Childhood asthma is associated with COPD and known asthma variants in COPDGene: a genome-wide association study

et al. 2018

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“…8,18 Other cohorts have shown that asthma and wheezy bronchitis are associated with COPD risk. 22 In the Childhood Asthma Management Program, 11% of 1,041 participants met spirometric criteria for COPD by age 30 years, and analysis of lung growth trajectories showed a subset with reduced lung growth. 5 The Aberdeen WHEASE cohort followed 330 subjects to age 61 years, showing that childhood asthma and wheeze were associated with COPD development.…”

Section: Discussionmentioning

confidence: 99%

“…We demonstrate that among a population of adult smokers, asthma in early life results in more active respiratory disease, with increased frequency and severity of exacerbations but without an increased rate of lung function decline or disease progression on chest CT scans. 22 Early-life respiratory diseases are known risk factors for the development of COPD. [1][2][3][4][5] COPD in these populations is likely due to lung development progressing along a reduced lung growth trajectory, with maximal expected FEV 1 never being achieved.…”

Section: Discussionmentioning

confidence: 99%

Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline

Hayden

Hardin

Qiu

et al. 2018

Chest

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“…Some patients with NA exhibited a poor response to treatment and may have irreversible air ow obstruction [3]. A long-term cohort study has shown that children with asthma reported a 10-32-fold increased risk of developing adult COPD which was also characterized by airway neutrophilic in ammation [4]. Airway remodeling is a common pathological process of asthma and COPD and it is also an important cause of air ow limitation.…”

Section: Introductionmentioning

confidence: 99%

Soluble advanced glycosylation receptor is a potential target for the treatment of neutrophilic asthma

Zhang¹,

Xie²,

Sun³

et al. 2020

Preprint

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Background Neutrophilic asthma (NA) was a subtype of asthma. Soluble advanced glycosylation receptor (sRAGE) was considered to be associated with the neutrophilic airway. However, the role of sRAGE in NA still limited. Methods A NA mouse model was established and the levels of sRAGE in the bronchoalveolar lavage fluid (BALF) were measured by ELISA. Hematoxylin-eosin (HE) and Masson trichrome staining were used to identifying airway remodeling. Adeno-associated virus 9 (AAV9) overexpressed sRAGE and inhibitors for HMGB1, RAGE, and PI3K were used to intervene NA mouse model via tail-vein injection and intraperitoneally injection. Expressions of airway remodeling, EMT, and signaling markers were detected using qRT-PCR or western blotting. The levels of IL-17 and IL-6 in BALF were measured by ELISA. HMGB1 was applied to induce EMT of human bronchial epithelial cells (16HBE), then E-cadherin and vimentin expressions were examined after sRAGE, RAGE inhibitor, and PI3K inhibitor administration. Results sRAGE levels were significantly reduced in BALF and the airway remodeling was observed in the NA mouse model. AAV9-sRAGE significantly inhibited the neutrophilic airway inflammation, airway remodeling, and the expression of IL-17, IL-6, TGF-β1, RAGE, PI3K, and EMT markers -E-cadherin and vimentin in vivo. HMGB1 inhibitor, RAGE inhibitor, and PI3K inhibitor upregulated E-cadherin level. Moreover, HMGB1 promoted the EMT process via RAGE/PI3K in 16HBE cells and sRAGE reversed HMGB1- induced EMT in vitro. Conclusion sRAGE levels decrease in the mouse model with NA. sRAGE treatment attenuates neutrophilic airway inflammation, airway remodeling, and EMT. This suggests sRAGE may yield benefits in the treatment of NA.

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Childhood asthma is a risk factor for the development of chronic obstructive pulmonary disease

Cited by 60 publications

References 46 publications

Childhood asthma is associated with COPD and known asthma variants in COPDGene: a genome-wide association study

Childhood asthma is associated with COPD and known asthma variants in COPDGene: a genome-wide association study

Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline

Soluble advanced glycosylation receptor is a potential target for the treatment of neutrophilic asthma

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