<scp>IL</scp>‐33 induces production of autoantibody against autologous respiratory epithelial cells: a potential mechanism for the pathogenesis of <scp>COPD</scp>

Li, Qin; Hu, Yue; Chen, Yan; Lv, Zhe; Wang, Jingjing; An, Gary; Du, Xinyue; Wang, Huating; Corrigan, Chris J.; Wang, Wei; Ying, Sun

doi:10.1111/imm.13054

Cited by 15 publications

(9 citation statements)

References 39 publications

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“…IL-33 increases IL-13 production and results in airway mucus formation. Recently, Li and colleagues [ 17 ] showed that IL-33 induces production of autoantibodies against respiratory epithelial cells, which can be a potential mechanism for inflammation and alveolar destruction in COPD.…”

Section: Discussionmentioning

confidence: 99%

Association between plasma interleukin-33 level and acute exacerbation of chronic obstructive pulmonary disease

et al. 2021

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Background The role of interleukin (IL)-33 in patients with chronic obstructive pulmonary disease (COPD) has not been well elucidated. The aim of this study is to analyze the association between plasma IL-33 level and acute exacerbation of COPD. Methods Plasma IL-33 was measured in 62 COPD patients during their stable state. Patients were prospectively followed up for 1 year. The expression of IL-33 was measured in lung tissue obtained from 38 patients who underwent surgery. Results The number of exacerbations was significantly higher in the high plasma IL-33 group compared with the low plasma IL-33 group. On Poisson regression analysis, high plasma IL-33 was associated with increased risk of exacerbation (incidence rate ratio = 2.166, P = 0.043). The expression of IL-33 in the lung was higher in COPD patients than in controls. The expression of IL-33 was significantly correlated with smoking pack years (R = 0.45, P < 0.01) and Forced expiratory volume in 1 s (%) (R = − 0.58, P < 0.01). Conclusion The plasma level of IL-33 in patients with COPD was significantly associated with the risk of exacerbation in prospective follow up. The expression of IL-33 in the lung was positively correlated with smoking and negatively correlated with lung function.

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Section: Discussionmentioning

confidence: 99%

Association between plasma interleukin-33 level and acute exacerbation of chronic obstructive pulmonary disease

et al. 2021

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“…In the respiratory tract, IL-33 is predominantly released from epithelial cells, alveolar type II epithelial cells, endothelial cells, mast cells, and fibroblasts − (Figure ). It serves as an “alarmin” following insult with inhaled stimuli such as allergens, infections, pollution, and cigarette smoke, which results in activation, migration, and recruitment of innate and adaptive immune cells including eosinophils, ILC2s, mast cells, T cells, natural killer T cells, macrophages, dendritic cells, and hematopoietic progenitor cells and production of type 2 (Th2) cytokines including IL-4, IL-5, and IL-13 (reviewed in refs , , and ).…”

Section: Introductionmentioning

confidence: 99%

IL-33 in Chronic Respiratory Disease: From Preclinical to Clinical Studies

Donovan

Hansbro

2019

ACS Pharmacol. Transl. Sci.

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IL-33 has been deorphanized as a member of the IL-1 family and has key roles as an alarmin and cytokine with potent capacity to drive type 2 inflammation. This has led to a plethora of studies surrounding its role in chronic diseases with a type 2 inflammatory component. Here, we review the roles of IL-33 in two chronic respiratory diseases, asthma and chronic obstructive pulmonary disease (COPD). We discuss the hallmark and paradigm-shifting studies that have contributed to our understanding of IL-33 biology. We cover animal studies that have elucidated the mechanisms of IL-33 and assessed the role of anti-IL-33 treatment and immunization against IL-33. We highlight key clinical evidence for the potential of targeting increased IL-33 in respiratory diseases including exacerbations, and we outline current clinical trials using an anti-IL-33 monoclonal antibody in asthma patients. Finally, we discuss some of the challenges that have arisen in IL-33 biology and highlight potential future directions in targeting this cytokine in chronic respiratory diseases.

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“…Additionally, plasma IL-33 levels positively correlate with the peripheral eosinophil count in COPD patients. 16…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 gene polymorphisms and chronic obstructive pulmonary disease in the Chinese Han population

Liu

et al. 2020

J Int Med Res

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Objective To investigate the relationship between interleukin (IL)-33 gene polymorphisms rs928413 and rs7044343 with chronic obstructive pulmonary disease (COPD) in the Chinese Han population. Method We assessed IL-33 rs928413 and rs7044343 polymorphisms by Sanger sequencing of PCR products amplified from the genomic DNA of 160 COPD patients and 123 healthy controls. Results There was no significant difference in the distribution of rs928413 AA, AG, or AA genotypes or rs7044343 CC, CT, or TT genotypes between the two groups. However, COPD patients had a significantly higher frequency of the rs928413 G allele G (14.1% vs 7.3%, respectively). This allele was significantly associated with susceptibility to COPD (odds ratio [OR]: 2.04, 95% confidence interval [CI]: 1.12–3.57). The rs928413 dominant inheritance model was associated with COPD susceptibility (OR: 2.08, 95%CI: 1.09–4.04). Conclusion The G allele of rs928413 and the rs928413 dominant inheritance model were associated with susceptibility to COPD in the Chinese Han population.

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IL‐33 induces production of autoantibody against autologous respiratory epithelial cells: a potential mechanism for the pathogenesis of COPD

Cited by 15 publications

References 39 publications

Association between plasma interleukin-33 level and acute exacerbation of chronic obstructive pulmonary disease

Association between plasma interleukin-33 level and acute exacerbation of chronic obstructive pulmonary disease

IL-33 in Chronic Respiratory Disease: From Preclinical to Clinical Studies

Interleukin-33 gene polymorphisms and chronic obstructive pulmonary disease in the Chinese Han population

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