Considerations for and Mechanisms of Adjunct Therapy in COPD

Mandru, Rachana; Zhou, Christine; Pauley, Rachel; Burkes, Robert

doi:10.3390/jcm10061225

Cited by 5 publications

(3 citation statements)

References 58 publications

(34 reference statements)

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“…In COPD, vitamin D metabolism may be dysregulated with impaired conversion of 25(OH)D 3 to the active form 1,25(OH) 2 D 3 [10 ▪▪ ], which may affect its role in immune cell function. For example, only the active form promotes the expression of innate defences such as regulating macrophage differentiation and promoting apoptosis responses to invading pathogens and noxious stimulants [11].…”

Section: The Role Of Vitamin D In the Pulmonary Systemmentioning

confidence: 99%

Vitamin D deficiency in chronic obstructive pulmonary disease

Mullin

Milne

2022

Current Opinion in Pulmonary Medicine

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Purpose of reviewThere is biological and epidemiological evidence supporting a role for vitamin D in the respiratory system, and vitamin D deficiency (VDD) may be associated with poor health outcomes in people with chronic obstructive pulmonary disease (COPD). This review summarizes recent findings relevant to the role of vitamin D in COPD.Recent findingsThe prevalence of VDD in people with COPD may be underestimated. Treatment of severe VDD [serum 25(OH)D3 < 10 ng/ml] may reduce the risk of COPD exacerbations. Vitamin D supplementation may also improve functional capacity and quality of life in people with COPD. However, there is no strong evidence that vitamin D supplementation slows the decline in lung function.SummaryAlthough there are many known associations between vitamin D and COPD outcomes, the causal nature of these associations and the precise benefits of vitamin D supplementation remain unclear. High-quality randomized controlled trials are necessary.

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Section: The Role Of Vitamin D In the Pulmonary Systemmentioning

confidence: 99%

Vitamin D deficiency in chronic obstructive pulmonary disease

Mullin

Milne

2022

Current Opinion in Pulmonary Medicine

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“…Small airway epithelial epithelial-mesenchymal transformation (EMT) is the main cause of COPD small airway wall thickening and fibrosis (Sohal 2017 ). In recent years, there are accumulating researches on COPD, the specific mechanisms of the pathogenesis of COPD remains to be elucidated, and there is still no effective prevention and treatment (Negewo et al 2015 ; Zhu et al 2018 ; Mandru et al 2021 ; Poole et al 2019 ).…”

Section: Introductionmentioning

confidence: 99%

The antioxidant N-acetylcysteine promotes immune response and inhibits epithelial-mesenchymal transition to alleviate pulmonary fibrosis in chronic obstructive pulmonary disease by suppressing the VWF/p38 MAPK axis

Zhu

Kang

et al. 2021

Mol Med

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Background/aim N-Acetylcysteine (NAC) demonstrates applications in the prevention of exacerbation of chronic obstructive pulmonary disease (COPD). COPD is often characterized by fibrosis of the small airways. This study aims at investigating the physiological mechanisms by which NAC might mediate the pulmonary fibrosis in COPD. Methods A total of 10 non-smokers without COPD and 10 smokers with COPD were recruited in this study, and COPD rat models were established. Cigarette smoke extract (CSE) cell models were constructed. The gain- or loss-of-function experiments were adopted to determine the expression of VWF and the extent of p38 MAPK phosphorylation, levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and immunoglobulins (IgG, IgM and IgA) in the serum of COPD rats and supernatant of alveolar epithelial cells and to detect cell invasion and migration and the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes. Results Expression of VWF and the extent of p38 MAPK phosphorylation were increased in COPD. NAC inhibited p38 MAPK phosphorylation by reducing the VWF expression. NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-α in CSE cells and serum of COPD rats. NAC promoted immune response and suppressed epithelial-mesenchymal transformation (EMT) to relieve COPD-induced pulmonary fibrosis in vitro and in vivo by inhibiting the VWF/p38 MAPK axis. Conclusions Collectively, NAC could ameliorate COPD-induced pulmonary fibrosis by promoting immune response and inhibiting EMT process via the VWF/p38 MAPK axis, therefore providing us with a potential therapeutic target for treating COPD.

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“…The final article in this Issue raises the role of adjunct therapy in COPD [ 38 ]. The authors discussed the benefits and limitations for adding other therapies to routine COPD management.…”

mentioning

confidence: 99%