Chronic osteomyelitis diagnosis using MRI: optimising radiomics models through multi-level region of interest extensions.

Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disorder affecting approximately 10% of the global population. By 2025, the prevalence of COPD among individuals aged 25 and older is projected to rise to approximately 23% (, ). Anxiety and depression are common comorbidities in patients with COPD and are associated with an increased risk of acute exacerbations. Research has identified anxiety and depression as independent risk factors for these exacerbations, contributing to prolonged hospital stays and adverse prognostic outcomes (). Galectin-3 (Gal-3), a β-galactoside-binding lectin, plays a pivotal role in inflammation, fibrosis, and immune regulation. Evidence indicates that Gal-3 expression is upregulated in both the serum and lung tissue of patients with COPD. These elevated levels are closely correlated with the severity of airflow limitation, the frequency of acute exacerbations, and disease progression, suggesting that Gal-3 is a critical mediator in chronic airway inflammation and remodeling (). Furthermore, Gal-3 possesses the ability to cross the blood-brain barrier, activate central microglia, and promote neuroinflammation a core mechanism underlying psychiatric disorders such as depression and anxiety (). This suggests that Gal-3 may serve as a potential molecular bridge linking peripheral inflammation in COPD to central nervous system dysfunction. The equilibrium between T helper 1 (Th1) and T helper 2 (Th2) cells is fundamental to the maintenance of immune homeostasis. A hallmark of COPD is a Th1/Th2 immune imbalance, characterized primarily by the excessive activation of Th1-type immune responses. Th1 dominance typically manifests as the upregulation of Th1 cells and associated cytokines, which subsequently activate macrophages, recruit neutrophils, and promote the release of proinflammatory mediators such as tumor necrosis factor-α (TNF-α). This cascade drives persistent chronic airway inflammation, tissue destruction, and airway remodeling, thereby acting as a key driver of inflammatory progression in COPD (). While Th2 immune responses are relatively weaker in classic COPD, they are not entirely absent. Studies indicate that Th2 cytokines, such as interleukin-4 (IL-4), are elevated in a subset of COPD patients and may contribute to disease heterogeneity by promoting mucus hypersecretion and eosinophilic inflammation (). In this study, IL-2, IFN-γ, IL-4 and IL-33 were selected from numerous Th1/Th2 cytokines as detection indicators based on the following: IL-2 is a key factor that drives the proliferation and differentiation of T cells, and it can reflect the activation intensity of Th1 immune response (). Moreover, it is significantly correlated with depressive symptoms in patients with COPD (). IFN-γ, as the characteristic effector molecule of Th1-type immunity, shows a dominant expression in the pulmonary inflammation of COPD and participates in neuronal apoptosis (). IL-4 is a key upstream factor that initiates Th2 differentiation and is regarded as a sensitive indicator of Th2 response deviation (). Although IL-33 is not a traditional Th2 differentiation factor, as an “alarm signal” released by airway epithelium, it can strongly promote Th2-type immune responses and airway inflammation (). The above four factors collectively cover the classic Th1/Th2 pathway and the epithelial-immune interconnection pathway, and can comprehensively reflect the Th1/Th2 immune imbalance state in COPD and its potential neuro-immune effects.