Biomass-related PM2.5 induced inflammatory microenvironment via IL-17F/IL-17RC axis

He, Fang; Yu, Xiaoyuan; Zhang, Jiahuan; Cui, Jieda; Tang, Lei; Zou, Siqi; Pu, Jinding; Ran, Pixin

doi:10.1016/j.envpol.2023.123048

Cited by 2 publications

(1 citation statement)

References 79 publications

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“…The most significant genetic risk factor for COPD is mutations in the SERPINA1 gene, which leads to congenital a1-antitrypsin deficiency (AATD) [6]. Smoking, exposure to biomass, occupational dust, air pollution, body infections, and advancing age all represent significant risk factors for the development of COPD [7][8][9][10][11][12]. The World Health Organisation reported that COPD was the third leading cause of death globally in 2019 [13].…”

Section: Introductionmentioning

confidence: 99%

Incremental long-term benefit of drug therapies for chronic obstructive pulmonary disease in quality of life but not mortality: a network meta-analysis

Pan,

Sun,

Gao

et al. 2024

Arch Med Sci

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IntroductionThe latest evidence revealed that dupilumab, an interleukin-4 (IL-4) and interleukin-13 (IL-13) blocker, significantly reduces the exacerbation risk in patients with chronic obstructive pulmonary disease (COPD). The efficacy of dupilumab compared with conventional inhaled drugs remains incompletely determined. This study aimed to investigate the comparative efficacy of dupilumab and conventional inhaled drugs in patients with stable COPD.Material and methodsThis study retrieved randomised clinical trials (RCTs) with follow-up ≥ 48 weeks on long-acting β-agonists (LABAs), long-acting muscarinic receptor antagonists (LAMAs), inhaled corticosteroids (ICSs), and dupilumab in the PubMed, EMBASE, and Cochrane Central Register of Controlled Trials databases. The information on eligible studies was extracted after the screening. The comparative efficacy of 4 drugs and their combinations in acute exacerbation and mortality was assessed using Bayesian network meta-analysis models.ResultsThis network meta-analysis identified 69 eligible RCTs on 7 classes of drug therapies after stepwise screening and included 125,331 COPD patients. Compared with placebo, the 7 drug interventions significantly reduced the risk of acute exacerbation, and the reduction degree increased with the incremental use of drug classes. ICS/LABA/LAMA/dupilumab was the most effective in decreasing exacerbation risk (OR = 0.561 [95% CI: 0.387–0.810]), followed by ICS/LABA/LAMA (OR = 0.717 [95% CI: 0.626–0.817]). The 7 drug therapies were not significantly associated with a lower risk of death compared to placebo. Nevertheless, ICS/LABA/LAMA/dupilumab is the most likely to be effective in decreasing mortality.ConclusionsThe incremental use of combinations of conventional and novel drugs contributed to the long-term benefits in acute exacerbation but not death in COPD. The optimal drug combination in terms of acute COPD exacerbation was ICS/LABA/LAMA/dupilumab.

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Section: Introductionmentioning

confidence: 99%

Incremental long-term benefit of drug therapies for chronic obstructive pulmonary disease in quality of life but not mortality: a network meta-analysis

Pan,

Sun,

Gao

et al. 2024

Arch Med Sci

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Advances in understanding the role of interleukins in pulmonary fibrosis (Review)

He,

Shen,

Zhai

et al. 2024

Exp Ther Med

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Pulmonary fibrosis (PF) is a progressive, irreversible disease characterized by heterogeneous interstitial lung tissue damage. It originates from persistent or repeated lung epithelial injury and leads to the activation and differentiation of fibroblasts into myofibroblasts. Interleukins (ILs) are a group of lymphokines crucial for immunomodulation that are implicated in the pathogenesis of PF. However, different types of ILs exert disparate effects on PF. In the present review, based on the effect on PF, ILs are classified into three categories: i) Promotors of PF; ii) inhibitors of PF; and iii) those that exert dual effects on PF. Several types of ILs can promote PF by provoking inflammation, initiating proliferation and transdifferentiation of epithelial cells, exacerbating lung injury, while other ILs can inhibit PF through suppressing expression of inflammatory factors, modulating the Th1/Th2 balance and autophagy. The present review summarizes the association of ILs and PF, focusing on the roles and mechanisms of ILs underlying PF.

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Biomass-related PM2.5 induced inflammatory microenvironment via IL-17F/IL-17RC axis

Cited by 2 publications

References 79 publications

Incremental long-term benefit of drug therapies for chronic obstructive pulmonary disease in quality of life but not mortality: a network meta-analysis

Incremental long-term benefit of drug therapies for chronic obstructive pulmonary disease in quality of life but not mortality: a network meta-analysis

Advances in understanding the role of interleukins in pulmonary fibrosis (Review)

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