Activity of sputum p38 MAPK is correlated with airway inflammation and reduced FEV1 in COPD patients

Cui-ping, Huang; Xie, Moying; Xin-hua, HE; Gao, Hui

doi:10.12659/msm.889880

Cited by 26 publications

(10 citation statements)

References 42 publications

(60 reference statements)

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“…In our study, both sUA levels and sUA/creatinine ratios were significantly higher in COPD patients than in healthy controls. It has been suggested that sUA levels increase in the presence of persistent systemic inflammation caused by COPD [23]. Interestingly, sUA levels and sUA/creatinine ratios were not associated with the severity of COPD in our study.…”

Section: Discussioncontrasting

confidence: 70%

Serum Uric Acid Levels and Uric Acid/Creatinine Ratios in Stable Chronic Obstructive Pulmonary Disease (COPD) Patients: Are These Parameters Efficient Predictors of Patients at Risk for Exacerbation and/or Severity of Disease?

et al. 2016

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BackgroundSerum uric acid (sUA) levels were previously found to be correlated with hypoxic states. We aimed to determine the levels of sUA and sUA/creatinine ratios in stable COPD patients and to evaluate whether sUA level and sUA/creatinine ratio can be used as predictors of exacerbation risk and disease severity.Material/MethodsThis cross-sectional study included stable COPD patients and healthy controls. The sUA levels and sUA/creatinine ratios in each group were evaluated and their correlations with the study parameters were investigated. ROC analyses for exacerbation risk and disease severity were reported.ResultsThe study included 110 stable COPD patients and 52 healthy controls. The mean sUA levels and sUA/creatinine ratios were significantly higher in patients with COPD compared to healthy controls. The most common comorbidities in COPD patients were hypertension, diabetes, and coronary artery disease. While sUA levels were significantly higher in patients with hypertension (p=0.002) and malignancy (p=0.033), sUA/creatinine ratios was higher in patients with malignancy (p=0.004). The ROC analyses indicated that sUA/creatinine ratios can be more useful than sUA levels in predicting exacerbation risk (AUC, 0.586 vs. 0.426) and disease severity (AUC, 0.560 vs. 0.475) especially at higher cut-off values, but with low specificity.ConclusionsOur study suggested that sUA levels and sUA/creatinine ratios increased in patients with stable COPD, especially among patients with certain comorbidities compared to healthy controls. At higher cut-off values, sUA levels and especially sUA/creatinine ratios, might be useful in predicting COPD exacerbation risk and disease severity. Also, their association with comorbidities, especially with malignancy and hypertension, may benefit from further investigation.

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Section: Discussioncontrasting

confidence: 70%

Serum Uric Acid Levels and Uric Acid/Creatinine Ratios in Stable Chronic Obstructive Pulmonary Disease (COPD) Patients: Are These Parameters Efficient Predictors of Patients at Risk for Exacerbation and/or Severity of Disease?

et al. 2016

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“…8 In this regard, it is noteworthy that high sputum levels of phospho-p38 MAPK can be detected in COPD patients. 42 Furthermore, such an enhanced activity of p38 MAPK was closely associated with several biological and lung functional parameters, including high concentrations of sputum neutrophils and IL-8, as well as low values of forced expiratory volume in one second (FEV 1 ). 42 Taken together, the above findings suggest that in COPD p38 MAPK activation is markedly correlated with both pulmonary inflammation and the progressive deterioration of respiratory function.…”

Section: Role Of P38 Mapk In Copd Pathophysiologymentioning

confidence: 98%

Role of p38 Mitogen-Activated Protein Kinase in Asthma and COPD: Pathogenic Aspects and Potential Targeted Therapies

Pelaia¹,

Vatrella²,

Gallelli³

et al. 2021

DDDT

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Among the various members of the mitogen-activated protein kinase (MAPK) family, p38 MAPK subgroup is the most involved in airway and lung inflammation underlying asthma and chronic obstructive pulmonary disease (COPD). In particular, several environmental agents including aeroallergens, cigarette smoke, airborne pollutants, viral and bacterial pathogens activate the p38α isoform which in turn up-regulates the expression of multiple proinflammatory cytokines and chemokines, as well as the production of some fibrogenic factors. Therefore, p38 MAPK-induced bronchial inflammation and remodelling significantly contribute to the development, persistence and amplification of airflow limitation, which is the hallmark of asthma and COPD. Such advances in our understanding of p38 role in the pathobiology of the above widespread, chronic obstructive respiratory diseases, have led to consider p38 MAPK as a suitable molecular target for novel treatment strategies. Indeed, many studies have been carried out in both animal and clinical settings, with the aim of evaluating the potential therapeutic effects of p38 MAPK inhibitors in both asthma and COPD.

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“… 243 Each subtype of p38MAPK has unique functions due to differential expression across tissue types and different regulatory kinases and downstream genes, hence their targeting comes with adverse effects. Although some clinical trials are in progress, due to severe side effects such as those caused by an undesired pharmacological activity, suppression of the innate immune response to viral and bacterial infections, and damage to the central nervous system and liver, 244 , 245 these drugs remain challenging for a clinical application. There is a need to develop inhaled formulations and selective inhibitors of the α-δ subgroups.…”

Section: New Molecular Targeted Drugsmentioning

confidence: 99%

Progress in the mechanism and targeted drug therapy for COPD

Wang

Zhou

Wang

et al. 2020

Sig Transduct Target Ther

140

117

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Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, have significant therapeutic effects; however, they also cause side effects, including infection and immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. The mechanism by which Trx affects COPD is different from glucocorticoid-based mechanisms which regulate the inflammatory reaction in association with suppressing immune responses. In addition, Trx also improves the insensitivity of COPD to steroids by inhibiting the production and internalisation of macrophage migration inhibitory factor (MIF). Taken together, these findings suggest that Trx may be the ideal drug for treating COPD.

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Activity of sputum p38 MAPK is correlated with airway inflammation and reduced FEV1 in COPD patients

Cited by 26 publications

References 42 publications

Serum Uric Acid Levels and Uric Acid/Creatinine Ratios in Stable Chronic Obstructive Pulmonary Disease (COPD) Patients: Are These Parameters Efficient Predictors of Patients at Risk for Exacerbation and/or Severity of Disease?

Serum Uric Acid Levels and Uric Acid/Creatinine Ratios in Stable Chronic Obstructive Pulmonary Disease (COPD) Patients: Are These Parameters Efficient Predictors of Patients at Risk for Exacerbation and/or Severity of Disease?

Role of p38 Mitogen-Activated Protein Kinase in Asthma and COPD: Pathogenic Aspects and Potential Targeted Therapies

Progress in the mechanism and targeted drug therapy for COPD

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