Xiaolin Chen

Background: Mycoplasma pneumoniae (MP) is a key pathogen causing pediatric community‐acquired pneumonia. Increasing macrolide resistance poses considerable clinical challenges. This study investigated MP epidemiology and macrolide resistance in children aged 0–14 years in Southwest China from 2021–2025. Methods: Retrospective analysis of MP antibody, nucleic acid, and resistance gene detection data. MP infections were categorized into macrolide‐resistant (MRMP) and macrolide‐sensitive (MSMP) groups. Clinical information was collected and compared. Results: Positive rates for MP‐RNA, DNA, IgM, and total antibodies were 12.43%, 9.82%, 30.19%, and 49.82%, respectively. Infections predominantly affected children aged 2–8 years. The macrolide resistance rate was 87.87%. Compared with the MSMP group, the MRMP group had longer hospital stays (+0.74 days), higher rates of fiberoptic bronchoscopy (+19.6%), and a significantly higher initial macrolide treatment failure rate, leading to increased doxycycline use (+20.8%). Conclusion: MRMP infections are highly prevalent in Southwest China and are associated with more complex clinical conditions and worse outcomes. Early resistance gene detection is recommended for hospitalized children with suspected MP infection during epidemic seasons. For children aged 2–8 years with persistent high fever and imaging findings of lung consolidation or mucus plugs, high suspicion of MRMP is warranted, and timely fiberoptic bronchoscopy should be considered.

This study evaluated serum eosinophil cationic protein (ECP) as a biomarker for pediatric allergic airway diseases. A cross-sectional analysis was performed on children (1–17 years) with allergic asthma (AA, n = 124), allergic rhinitis (AR, n = 74), acute bronchitis (AB, n = 72), and healthy controls (HC, n = 58). Serum ECP, total IgE, eosinophil counts, allergen sensitization, and lung function were measured. Diagnostic performance was assessed using receiver operating characteristic (ROC) curves, and correlations among biomarkers were examined. Compared with HC, serum ECP levels were significantly elevated across all disease groups (AA, AR, and AB), with a particularly marked difference observed between AA and AR patients (p < 0.0001). The combination of ECP and IgE significantly improved the diagnostic accuracy for AA (AUC = 0.9494) and AR (AUC = 0.9501). Higher ECP levels were associated with increased sensitization to specific inhalant allergens and impaired pulmonary function, particularly in small airway indices. Serum ECP reflects eosinophil-mediated airway inflammation and enhances diagnostic performance for pediatric AA and AR, supporting its role as an auxiliary biomarker in evaluating pediatric allergic airway diseases.

Introduction: Chemokines are crucial in the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis (LN). This study aimed to detect chemokines and chemokine‐related cytokines in SLE patients with and without LN, as well as healthy controls, to identify potential biomarkers for clinical diagnosis. Methods: Luminex technology was used to measure 40 chemokines and chemokine‐related cytokines in serum and urine samples from SLE patients under 18 years. Chemokine concentrations were compared, and their correlation with the SLE Disease Activity Index (SLEDAI) was evaluated. Diagnostic performance was assessed using receiver operating characteristic (ROC) curve analysis. Results: Significant differences in the serum levels of CCL22, CCL23, and CXCL13, and urine levels of CCL7, CCL19, CCL22, CXCL2, CXCL5, and CXCL13, as well as chemokine‐related cytokines IL‐2, IL‐4, TNF‐α, and GM‐CSF, were observed between the SLE, LN, and healthy control groups. CCL22 and CXCL13 exhibited specific expression in both serum and urine samples and were significantly correlated with SLEDAI. Diagnostic performance assessments show that CCL22 and CXCL13 have excellent diagnostic efficacy for both SLE and LN. Importantly, the combination of CCL22 and CXCL13 significantly improved the accuracy of SLE diagnosis and enhanced the differential diagnosis of LN. Conclusion: Our study suggests that the combined use of CCL22 and CXCL13 could serve as promising biomarkers for diagnosing SLE and LN.

TANK-binding kinase 1 (TBK1) is a key signaling kinase involved in innate immune and inflammatory responses. TBK1 drives immune cells to participate in the inflammatory response by activating the NF-κB and interferon regulatory factor signaling pathways in immune cells, promoting the expression of pro-inflammatory genes, and regulating immune cell function. Thus, it plays a crucial role in initiating a signaling cascade that establishes an inflammatory environment. In inflammation-related diseases, TBK1 acts as a bridge linking inflammation to immunity, metabolism, or tumorigenesis, playing an important role in the pathogenesis of immune-mediated inflammatory diseases, metabolic, inflammatory syndromes, and inflammation-associated cancers by regulating the activation of inflammatory pathways and the production of inflammatory cytokines in cells. In this review, we focused on the mechanisms of TBK1 in immune cells and inflammatory-related diseases, providing new insights for further studies targeting TBK1 as a potential treatment for inflammation-related diseases. Thus, optimizing and investigating highly selective cell-specific TBK1 inhibitors is important for their application in these diseases.