Here we show that we can use an established transgenic animal model of COPD based on inducible IL13-driven pulmonary emphysema (IL13<sup>TG</sup>) to interrogate the mechanisms of skeletal muscle dysfunction.
In some experiments, RV-infected COPD cells and mice with COPD phenotype were treated with γ-secretase inhibitor or interleukin-13 neutralising antibody and assessed for GCH.
An emerging scheme focuses on expansion of airway progenitor epithelial cells that feed forward for a type 2 immune response and consequent IL-13-driven mucus production that is linked to the morbidity and mortality of COPD.
Asthma and some cases of COPD are mainly driven by type 2 immune responses, which comprise increased airway eosinophils, T helper 2 (T<sub>H</sub>2) cells and group 2 innate lymphoid cells (ILC2s) and the secretion of IL-4, IL-5 and IL-13.
IL-6 has been shown to play an important role in chronic obstructive pulmonary disease (COPD), while IL-13 is described as one of the key mediators of allergic asthma.
Evidence for a positive association between the T allele of the IL-13 SNP rs1800925 and COPD risk was found in the overall population (odds ratio [OR] = 1.57, 95% confidence interval [95% CI]: 1.21-2.04, Pz = .001).
In humans with COPD, IL33 gene expression was also associated with IL13 and mucin gene expression, and IL33 induction was traceable to a subset of airway basal cells with increased capacities for pluripotency and ATP-regulated release of IL-33.
In contrast, 8/12 genes (early growth response factor 1, MMP1, MMP9, MMP10, plasminogen activator urokinase, plasminogen activator urokinase receptor, tumor necrosis factor, and IL13) increased and 4/12 (MMP2, tissue inhibitor of matrix metalloproteinase-1, collagen 1alpha1, and transforming growth factor-beta3) decreased in the surrounding lung tissue in association with progression of COPD.
We investigated whether single nucleotide polymorphisms (SNPs) in the IL13 pathway may contribute to the susceptibility and severity of asthma and COPD in adults.
Genetic variants of the two adjacent genes, IL13 and IL4 have frequently been reported as being associated with susceptibility to atopy and asthma, both in adults and children, and some studies also suggest association with lung function and chronic obstructive pulmonary disease.
This research was conducted to study the frequencies of IL-13 gene promoter 1055 (IL-13-1055) and TNF-alpha gene-308 polymorphisms in the patients with COPD and to investigate the effect of those genetic polymorphisms on COPD in the Chinese population.