Pathological Mechanism and Targeted Drugs of COPD

Guo, Ping; Li, Rui; Piao, Tie Hua; Wang, Chun Lan; Wu, Xiao Lu; Cai, Hong Yan

doi:10.2147/copd.s366126

Cited by 66 publications

(53 citation statements)

References 99 publications

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“…There is a close association between IL-5 and the aggregation and differentiation of eosinophil. Sputum levels of IL-5 in patients with stable COPD correlate with the degree of eosinophilia [6,7,10,12,[14][15][16].…”

Section: Players Involved In Inflammationmentioning

confidence: 99%

“…IL-8 also stimulates phagocytosis. In its target cells, IL-8 can increase intracellular Ca 2+ and the respiratory burst, which means the release of reactive oxygen species by macrophages and neutrophilic granulocytes during phagocytosis [6,7,[11][12][13]15]. IL-10 is mainly secreted by monocytes and T-lymphocytes.…”

Section: Players Involved In Inflammationmentioning

confidence: 99%

“…Oxidative stress also increases mucus production, the formation of proteases, and the migration of neutrophilic granulocytes into the bronchial mucosa. An oxidant-antioxidant imbalance also occurs in other lung diseases, such as pulmonary fibrosis or bronchial asthma [3,5,15,19].…”

Section: Forms Of Inflammation or Damagementioning

confidence: 99%

“…These include muscarinic antagonists, ß2-sympathomimetics, corticosteroids, mucolytics, antitussives, betablocker, N-acetyl-L-cysteine, antibiotics, oxygen, and vaccinations against pneumococcus infection, pertussis, influenza, and COVID-19. The administration of the phosphodiesterase-4 inhibitor roflumilast is possible as add-on therapy in patients with COPD who repeatedly exacerbate despite therapy, who are assigned to the chronic bronchitis phenotype, and who have an FEV1 (forced expiratory pressure in 1 s) <50% [2,3,15].…”

Section: Use Of Biologics In Refractory Therapy Of Copdmentioning

confidence: 99%

“…Benralizumab is a potential add-on therapy in adult patients with severe eosinophilic COPD as well as bronchial asthma. Application of benralizumab is subcutaneous injection [1,6,15,16].…”

Section: Use Of Biologics In Refractory Therapy Of Copdmentioning

confidence: 99%

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COPD and Inflammation

Peiser¹

2023

A Compendium of Chronic Obstructive Pulmonary Disease

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COPD is associated with chronic inflammation of the airways, which causes damage to defense and repair mechanisms, resulting in remodeling processes in the bronchi and bronchioles. This leads to fibrosis of the lung tissue, increased smooth muscle tension, swelling of bronchial mucosa, loss of cilia function with accumulation of mucus, and finally to chronic pulmonary obstruction and possibly emphysema, with the main symptoms of dyspnea, coughing, and expectoration. Inhaled pollutants can activate immune cells like macrophages, T-lymphocytes, and subsequently neutrophilic granulocytes. Together, they release various pro-inflammatory messenger substances and enzymes. As a relevant example, they secrete proteases and disable antiproteases, an imbalance that destabilizes lung tissue. Of particular importance are several cytokines that are significantly elevated in the plasma of patients with COPD signals. In addition to the pathophysiologically clearly defined neutrophilic inflammation, there are also COPD patients with a predominantly eosinophilic inflammation, which could overlap with allergic bronchial asthma. Furthermore, inhaled pollutants can lead to oxidative stress, which increases inflammation and remodeling. Respiratory infections, in most cases bacterial infections, can trigger an exacerbation of already established COPD, in most cases bacterial infections. In addition to conventional medication, in case of refractory therapy, treatment with biologics could be an option.

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Section: Players Involved In Inflammationmentioning

confidence: 99%

Section: Players Involved In Inflammationmentioning

confidence: 99%

Section: Forms Of Inflammation or Damagementioning

confidence: 99%

Section: Use Of Biologics In Refractory Therapy Of Copdmentioning

confidence: 99%

“…Benralizumab is a potential add-on therapy in adult patients with severe eosinophilic COPD as well as bronchial asthma. Application of benralizumab is subcutaneous injection [1,6,15,16].…”

Section: Use Of Biologics In Refractory Therapy Of Copdmentioning

confidence: 99%

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COPD and Inflammation

Peiser¹

2023

A Compendium of Chronic Obstructive Pulmonary Disease

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Regulatory roles of Osteopontin in lung epithelial inflammation and epithelial‐telocyte interaction

Fu,

Liu,

Shi

et al. 2023

Clinical & Translational Med

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BackgroundLung epithelial cells play important roles in lung inflammation and injury, although mechanisms remain unclear. Osteopontin (OPN) has essential roles in epithelial damage and repair and in lung cancer biological behaviours. Telocyte (TC) is a type of interstitial cell that interacts with epithelial cells to alleviate acute inflammation and lung injury. The present studies aim at exploring potential mechanisms by which OPN regulates the epithelial origin lung inflammation and the interaction of epithelial cells with TCs in acute and chronic lung injury.MethodsThe lung disease specificity of OPN and epithelial inflammation were defined by bioinformatics. We evaluated the regulatory roles of OPN in OPN‐knockdown or over‐expressed bronchial epithelia (HBEs) challenged with cigarette smoke extracts (CSE) or in animals with genome OPN knockout (gKO) or lung conditional OPN knockout (cKO). Acute lung injury and chronic obstructive pulmonary disease (COPD) were induced by smoking or lipopolysaccharide (LPS). Effects of OPN on PI3K subunits and ERK were assessed using the inhibitors. Spatialization and distribution of OPN, OPN‐positive epithelial subtypes, and TCs were defined by spatial transcriptomics. The interaction between HBEs and TCs was assayed by the co‐culture system.ResultsLevels of OPN expression increased in smokers, smokers with COPD, and smokers with COPD and lung cancer, as compared with healthy nonsmokers. LPS and/or CSE induced over‐production of cytokines from HBEs, dependent upon the dysfunction of OPN. The severity of lung inflammation and injury was significantly lower in OPN‐gKO or OPN‐cKO mice. HBEs transferred with OPN enhanced the expression of phosphoinositide 3‐kinase (PI3K)CA/p110α, PIK3CB/p110β, PIK3CD/p110δ, PIK3CG/p110γ, PIK3R1, PIK3R2 or PIK3R3. Spatial locations of OPN and OPN‐positive epithelial subtypes showed the tight contact of airway epithelia and TCs. Epithelial OPN regulated the epithelial communication with TCs, and the down‐regulation of OPN induced more alterations in transcriptomic profiles than the up‐regulation.ConclusionOur data evidenced that OPN regulated lung epithelial inflammation, injury, and cell communication between epithelium and TCs in acute and chronic lung injury. The conditional control of lung epithelial OPN may be an alternative for preventing and treating epithelial‐origin lung inflammation and injury.

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Indole-3-Aldehyde alleviates lung inflammation in COPD through activating Aryl Hydrocarbon Receptor to inhibit HDACs/NF-κB/NLRP3 signaling pathways

Wang,

Tao,

et al. 2024

J Mol Med

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Pathological Mechanism and Targeted Drugs of COPD

Cited by 66 publications

References 99 publications

COPD and Inflammation

COPD and Inflammation

Regulatory roles of Osteopontin in lung epithelial inflammation and epithelial‐telocyte interaction

Indole-3-Aldehyde alleviates lung inflammation in COPD through activating Aryl Hydrocarbon Receptor to inhibit HDACs/NF-κB/NLRP3 signaling pathways

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