Meiqi Li

Eosinophils are key immunopathological cells in respiratory diseases and contribute to airway inflammation, tissue remodeling, and disease heterogeneity. Although eosinophils have traditionally been regarded as biomarkers of type 2 inflammation, increasing evidence indicates that they also function as active mediators of lung function impairment in selected respiratory diseases, including chronic obstructive pulmonary disease, asthma, and eosinophilic pneumonia. These disorders were selected because they represent distinct yet complementary models of eosinophil-associated airway and parenchymal injury, allowing comparison of shared and disease-specific mechanisms. Mechanistically, eosinophils impair lung function through the coordinated release of cytotoxic granule proteins, reactive oxygen species, lipid mediators, and cytokines, while interacting with epithelial, immune, and structural cells to amplify inflammation, airway remodeling, and tissue injury. These advances have improved understanding of eosinophil biology and facilitated the development of clinically relevant biomarkers and targeted therapies. Blood and sputum eosinophil counts remain the most widely used biomarkers, whereas emerging biomarkers, including eosinophil-derived neurotoxin, may further improve disease stratification and treatment monitoring. Biologics targeting interleukin-5 and its receptor have demonstrated therapeutic benefit in selected eosinophilic respiratory diseases, although treatment responses differ among disease phenotypes. This review summarizes current evidence regarding the molecular mechanisms linking eosinophils to lung function impairment, discusses the evolving role of eosinophils as both biomarkers and pathogenic drivers, and highlights the biomarker and therapeutic implications for precision management of respiratory diseases.

Objectives This study aimed to examine the diagnostic and prognostic value of the platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR) in patients with polymyositis/dermatomyositis (PM/DM). Method Clinical data of 200 patients with PM/DM and 204 healthy controls were retrospectively reviewed. We examined whether the PLR and NLR were associated with PM/DM. Results The PLR and NLR were higher in patients with PM/DM than in controls (both P < 0.001). The PLR and NLR were higher in patients with DM than in those with PM (both P < 0.01). The PLR was higher in the anti-melanoma differentiation-associated protein-5 (anti-MDA5) ⁺ PM/DM group than in the anti-MDA5^- PM/DM group (P = 0.002). The NLR in non-survivors was higher than that in survivors (P = 0.01). The NLR was positively correlated with the occurrence of interstitial lung disease (ILD). The PLR and NLR were independent predictors of PM/DM, as well as risk factors (both P < 0.001). Moreover, the NLR had a predictive value for PM/DM-ILD and was closely related to mortality (P = 0.033, P = 0.003, respectively). Conclusions Patients with PM/DM have a higher NLR and PLR than healthy controls, especially in those with anti-MDA5⁺. The PLR and NLR are independent risk factors for PM/DM and have some predictive value. The NLR is correlated with ILD and associated with an increased risk of mortality in patients with PM/DM. The NLR and PLR may be simple, economical, and accurate diagnostic and prognostic markers for patients with PM/DM. Key points • The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been studied in numerous inflammatory diseases as potential markers, but their clinical significance in polymyositis/dermatomyositis (PM/DM) remains unclear. • We examined the changes in the NLR and PLR between patients with PM/DM and healthy controls, as well as their association with mortality, interstitial lung disease, and anti-melanoma differentiation-associated protein-5. • Patients with PM/DM may benefit from using the NLR and PLR as simple, economical, and accurate diagnostic and prognostic markers.

Connective tissue disease (CTD) patients may suffer from pulmonary arterial hypertension (PAH), a serious complication, and anti-U1 ribonucleoprotein (RNP) antibodies can be used as a potential indicator for the development and prognosis of CTD-associated PAH (CTD-PAH). However, there are still some controversies; thus, a systematic review and meta-analysis were performed. We searched PubMed, Embase, Cochrane Library, and Scopus for eligible studies and assessed their quality using Newcastle–Ottawa scales or Agency for Healthcare Research and Quality indicators according to the type of research. Odds ratio (OR) was adopted as a measure of effect in risk factor analysis, and hazard ratio (HR) was adopted for prognostic factor analysis. Publication bias was evaluated using the Egger’s test. Thirteen studies were finally included. Anti-U1 RNP antibody was proved as a risk factor for PAH among CTD patients (OR = 5.30, 95%CI 2.96–9.48, p < 0.05) and a protective factor against mortality among CTD-PAH patients (HR = 0.55, 95%CI 0.36–0.83, p < 0.05). CTD patients with positive anti-U1 RNP antibodies are at high risk for PAH, so routine screening examinations, including echocardiography, are recommended. Additionally, anti-U1 RNP positivity has been linked to decreased mortality in patients with CTD-PAH.

Zhang Q, et al. Yonsei Med J. 2022 Feb;63(2):148-157. https://doi.org/10.3349/ymj.2022.63.2.148