Circulating eosinophil levels and lung function decline in stable chronic obstructive pulmonary disease: a retrospective longitudinal study

Ferrari, Marcello; Pizzini, Michela; Cazzoletti, Lucia; Ermon1, Valentina; Marchi, Sergio De; Carbonare, Luca Dalle; Crisafulli, Ernesto; Spelta, Francesco

doi:10.36416/1806-3756/e20220183

Cited by 2 publications

(2 citation statements)

References 35 publications

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“…Neutrophil counts in COPD display heterogeneity across different respiratory system locations. Inflammation, immune response, and bacterial infection contribute to increased neutrophil counts in the airways, bronchi, bronchial epithelium [99], mucous glands, BAL fluid [98,100], and sputum samples of COPD patients [98,[101][102][103]. Neutrophil counts in peripheral blood can be either increased or normal, depending on the disease phase [102].…”

Section: Neutrophilsmentioning

confidence: 99%

“…Inflammation, immune response, and bacterial infection contribute to increased neutrophil counts in the airways, bronchi, bronchial epithelium [99], mucous glands, BAL fluid [98,100], and sputum samples of COPD patients [98,[101][102][103]. Neutrophil counts in peripheral blood can be either increased or normal, depending on the disease phase [102]. The systemic nature of neutrophilic inflammation in COPD suggests involvement beyond localized regions.…”

Section: Neutrophilsmentioning

confidence: 99%

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p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics

Ahmadi,

Ahrari,

Salimian

et al. 2023

Cell Commun Signal

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Background Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar remodeling. Although the abnormalities are primarily prompted by chronic exposure to inhaled irritants, maladjusted and self-reinforcing immune responses are significant contributors to the development and progression of the disease. The p38 isoforms are regarded as pivotal hub proteins that regulate immune and inflammatory responses in both healthy and disease states. As a result, their inhibition has been the subject of numerous recent studies exploring their therapeutic potential in COPD. Main body We performed a systematic search based on the PRISMA guidelines to find relevant studies about P38 signaling in COPD patients. We searched the PubMed and Google Scholar databases and used “P38” AND “COPD” Mesh Terms. We applied the following inclusion criteria: (1) human, animal, ex vivo and in vitro studies; (2) original research articles; (3) published in English; and (4) focused on P38 signaling in COPD pathogenesis, progression, or treatment. We screened the titles and abstracts of the retrieved studies and assessed the full texts of the eligible studies for quality and relevance. We extracted the following data from each study: authors, year, country, sample size, study design, cell type, intervention, outcome, and main findings. We classified the studies according to the role of different cells and treatments in P38 signaling in COPD. Conclusion While targeting p38 MAPK has demonstrated some therapeutic potential in COPD, its efficacy is limited. Nevertheless, combining p38 MAPK inhibitors with other anti-inflammatory steroids appears to be a promising treatment choice. Clinical trials testing various p38 MAPK inhibitors have produced mixed results, with some showing improvement in lung function and reduction in exacerbations in COPD patients. Despite these mixed results, research on p38 MAPK inhibitors is still a major area of study to develop new and more effective therapies for COPD. As our understanding of COPD evolves, we may gain a better understanding of how to utilize p38 MAPK inhibitors to treat this disease.

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