Mycoplasma pneumoniae (MP) is a major cause of pediatric respiratory infections, characterized by cyclical epidemics and age- and season-specific patterns. However, long-term epidemiological data spanning multiple epidemic cycles are limited. We conducted a 20-year retrospective study of children (< 18 years) hospitalized with respiratory tract infections and undergoing MP testing at Children's hospital of Soochow University from October 2005 to December 2025. MP infection was defined by positive PCR and/or serological evidence. Positivity was analyzed by age, sex, season, calendar period, and COVID-19 pandemic phase. Among 51,399 specimens, 16,086 were MP-positive (31.30

BACKGROUND:Airway epithelial barrier dysfunction is a central feature of asthma pathogenesis, yet the molecular mechanisms by which post-translational modifications regulate epithelial integrity remain incompletely understood. Fucosylation has emerged as a potential regulator of epithelial homeostasis across mucosal tissues. OBJECTIVE:We sought to investigate whether epithelial fucosylation contributes to allergen-induced barrier dysfunction and airway inflammation and to define their underlying mechanisms. METHODS:Fucosylation levels were assessed in saliva from children with asthma using mass spectrometry. Air-liquid interface epithelial cultures were used to assess barrier function by transepithelial electrical resistance, tight junction protein expression and cytokine release. Transcriptomic analyses were performed to identify dysregulated fucosylation pathways. Fut1 was selectively inhibited in vivo and in vitro using intratracheally delivered AAV6-encoded shRNA. Downstream targets were also evaluated by RNA sequencing. RESULTS:Fucosylation was significantly increased in saliva from children with asthma and in allergen-exposed mouse airways. Pharmacologic inhibition of fucosylation preserved epithelial barrier integrity, maintained junctional organization and reduced allergen-induced epithelial cytokine release. Transcriptomic profiling identified fucosylation as a major upregulated pathway, with increased expression of Fut1, Fut2, Fut7 and Fut9. Epithelial-specific Fut1 knockdown attenuated Th2-driven inflammation, preserved epithelial junctional architecture and suppressed alarmin release. Integrated analyses revealed 56 Fut1-dependent genes enriched in cell-adhesion pathways, including Cdh12, App, Ank3 and Cd9. Fut1-CDH12 protein interaction was confirmed by immunoprecipitation, and FUT1-dependent induction of CDH12 disrupted epithelial junctional organization and barrier function. CONCLUSION:These findings identify the FUT1-CDH12 axis as a previously unrecognized epithelial mechanism promoting barrier dysfunction and allergic airway inflammation in asthma.

BACKGROUND:Obstructive sleep apnea (OSA) may induce chronic systemic inflammation, which may serve as a potential mechanism contributing to multiple complications. The timely identification of high inflammatory status (HIS) in pediatric OSA is crucial for effective clinical diagnosis and management. This study aimed to evaluate influencing factors in hsCRP levels, and further investigated the risk factors associated with HIS in pediatric OSA patients. METHODS:Children aged 3 to 15 years who presented with snoring symptoms and underwent polysomnography (PSG) at the sleep center were included in this study. All participants completed a comprehensive questionnaire, a physical examination, nasopharyngeal X-ray imaging and a blood test. The physical examination included measurements of height, weight, and visual evaluation of tonsillar hypertrophy. RESULTS:A total of 1,171 children were enrolled, with 562 cases diagnosed with OSA. Utilizing threshold for hsCRP generated via ROC curve, 299 and 872 children exhibited HIS and Low Inflammatory Status, respectively. Compared to the control group, the hsCRP levels in the OSA group were significantly elevated. Pediatric OSA with HIS had higher BMI and a greater proportion of both overweight and obese. Logistic regression analysis demonstrated that HIS was independently positively correlated with BMI and mean time of obstructive apnea, and negatively associated with minimum SpO2. CONCLUSIONS:HsCRP in pediatric OSA patients were notably elevated, whilst identifying BMI, mean time of obstructive apnea, and minimum SpO2 as independent factors leading to HIS. HsCRP may function as an effective blood index capable of identifying individuals exhibiting HIS linked to OSA.

Background: This study aimed to explore the mechanisms underlying T‐cell differentiation in asthma.Methods and Results: Flow cytometry was performed to detect Th cells. LC‐MS/MS was performed to assess lipid metabolism. HE staining was performed to assess the pathological changes of the lung tissues. ELISA was performed to detect cytokine levels. The results of quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blot showed that miR‐192‐5p expression was decreased, while SCD1 expression was increased in CD4+T cells isolated from the peripheral blood of children with asthma. The dual luciferase reporter assay determined the direct interaction between miR‐192‐5p and SCD1. MiR‐192‐5p inhibitor reduced ASCL3 and PPARα, increased FASN and SREBP1c mRNA expression and protein levels in mouse spleen CD4+T cells, and elevated Th2 and Th17 cells, but these effects were reversed by the SCD1 inhibitor. Oleic acid (OA) reduced Th1 cells and increased Th2 and Th17 cells in mouse spleen CD4+T cells treated with an SCD1 inhibitor. Additionally, pri‐miR‐192‐5p expression was increased in CD4+T cells isolated from the peripheral blood of asthmatic children, and the deletion of METTL3 upregulated pri‐miR‐192‐5p expression in an m6A‐dependent manner. MiR‐192‐5p mimic and inhibitor both reversed miR‐192‐5p and SCD1 expression affected by overexpression or deletion of METTL3, both in vivo and in vitro. Furthermore, METTL3 overexpression attenuated lung inflammation, elevated Th1 cells, and reduced Th2 and Th17 cells in CD4+T cells isolated from the peripheral blood of asthmatic mice. These effects were reversed by the miR‐192‐5p inhibitor.Conclusion: These results suggest that METTL3/miR‐192‐5p/SCD1 axis regulates lipid metabolism and affects T cell differentiation, thus affecting asthma progression. This study may provide novel insights into the pathogenesis of asthma and a new treatment strategy.

To investigate the genotyping and drug resistance of Mycoplasma pneumoniae (MP) epidemic strains in children and analyze the risk factors for refractory Mycoplasma pneumoniae pneumonia (RMPP). Nasopharyngeal aspirates (NPA) were collected from hospitalized children with MP infection from September to October 2023. Tracheoscopy was performed when necessary, and Bronchoalveolar Lavage Fluid (BALF) was collected. Polymerase Chain Reaction (PCR) capillary electrophoresis were used to detect respiratory pathogens, and a nested PCR based on the MP P1 gene monitored MP subtypes. The MP-23 S rRNA V region was amplified and sequenced. Clinical data and laboratory results were analyzed for RMPP risk factors. From 261 children diagnosed with Mycoplasma pneumoniae pneumonia (MPP), cough (100

The aim of this study was to investigate the clinical characteristics of severe pneumonia caused by human bocavirus (HBoV) infection to explore the associated risk factors. We conducted a retrospective review of data from children hospitalized with HBoV pneumonia. Based on the severity of pneumonia, patients were categorized into severe pneumonia and non-severe pneumonia groups. Clinical manifestations, laboratory examination results, chest imaging and pathogens were analyzed. Logistic regression was employed to identify the risk factors for severe HBoV pneumonia. A total of 334 patients were admitted, with 44 (13.17

Background:Pollen is a significant contributor to respiratory allergies worldwide, underscoring the importance of understanding its association with childhood sensitization to enhance clinical management. Objective:This study focuses on investigating the prevalence of various airborne pollens and their correlation with clinical characteristics of childhood respiratory allergic diseases in southeastern China. Methods:From November 2020 to October 2021, this research employed Durham monitoring samplers to collect airborne pollen. Simultaneously, skin prick tests (SPTs) were performed on children with respiratory allergic conditions at the Children's Hospital of Soochow University and standardised questionnaires are also administered to assess children's symptoms. Results:Over the course of November 2020 to October 2021, the study identified more than 36 pollen species. Notably, the spring season (March to May) exhibited the highest pollen concentrations, with Broussonetia accounting for 30.04% and Pinus for 26.38%. Similarly, the autumn months (September to October) saw prominent taxa like Humulus scandens (47.55%) and Gramineae (35.93%). Among the patients, a significant 92.7% exhibited positive reactions, with 81.7% showing sensitization to house dust mites (HMD), 17.8% to pollen, and 3.7% to Cockroach. Noteworthy the five most common pollens were observed for Bermuda (6.0%), Elm pollen (6.0%), Birch pollen (4.6%), and Mugwort (4.6%). The study indicated a substantial multisensitized ratio among pollen-sensitized patients in comparison to non-pollen-sensitized ones (97.4% vs 1.6%, P <0.001). Moreover, weekly total airborne pollen concentrations showed positive correlations with weekly admissions due to allergic rhinitis(AR)(r=0.642, P <0.001), bronchial asthma (BA) (r= 0.472, P<0.001), and the coexistence of AR and BA (r=0.485, P <0.001). Conclusion:The findings found that there were two peaks of pollen count in a year during March-May and September-October. The findings emphasize the critical role of specific airborne pollens in driving sensitization and exacerbating respiratory allergic diseases in children.

Background: Neutrophilic asthma is characterized by the predominant infiltration of neutrophils in airway inflammation. Objective: To explore the therapeutic potential of an antibody against the inducible T cell co-stimulator ligand (ICOSL) in a mouse model of neutrophilic asthma. Methods: Female BALB/c mice were randomly assigned to different groups. They were then injected with ovalbumin (OVA)/lipopolysaccharides (LPS) to induce neutrophilic asthma. The mice were then treated with either anti-ICOSL (the I group), control IgG (the G group), or no treatment (the N group). Additionally, a control group of mice received vehicle PBS and was labeled as the C group (n=6 per group). One day after the last allergen exposure, cytokine levels were measured in plasma and bronchoalveolar lavage fluid (BALF) using ELISA. After analyzing and categorizing BALF cells, the lung tissues were examined histologically and immunohistochemically. Results: Administering anti-ICOSL resulted in a significant decrease in the total number of inflammatory infiltrates and neutrophils found in BALF. Moreover, it led to a decrease in the levels of interleukin (IL)-6, IL-13, and IL-17 in both BALF and plasma. Additionally, there was an increase in IFN-gamma levels in the BALF of asthmatic mice (p<0.05 for all). Treatment with anti-ICOSL also reduced lung interstitial inflammation, mucus secretion, and ICOSL expression in asthmatic mice. Conclusion: The treatment of anti-ICOSL effectively improved lung interstitial inflammation and mucus secretion in mice with neutrophilic asthma by restoring the balance of Th1/Th2/Th17 responses. These findings indicate that blocking the ICOS/ICOSL signaling could be an effective way to manage neutrophilic asthma.

Objective: The aim of the study is to describe the season of RSV prevalence in China during the COVID-19 pandemic. Methods: This multicenter retrospective study analyzed the epidemiology of pediatric RSV infections and the possible factors contributing to its variations in China from January 1, 2019, to October 31, 2022. Results: A total of 872,565 children were included. During the pandemic, RSV detection rate increased across various regions, including South China, East China, Central China, and Northeast China. From 2019 to 2021, the detection rates of RSV showed an increasing trend among children aged <1 year, 1-2 years, and 3-5 years, but decreased in 2022. Among those tested positive for RSV, the proportion of children under 1 year old significantly decreased during the pandemic. The spring season of RSV in China in 2020 was shortened, and most regions experienced a summer season of RSV in 2021. This shift led to a year-round RSV outbreak throughout 2021. After April 2022, RSV positive rate significantly decreased, and no clear seasonal pattern was observed. Conclusion: Our study found that the COVID-19 pandemic has disrupted the seasonal pattern of RSV outbreaks in China, leading to increased RSV positive rate and off-season outbreaks.

Background Neonate lung injury is a common phenomenon after perinatal asphyxia.Objective To evaluate proteomic profiles of exosomes isolated from lung injury offspring serum after perinatal asphyxia.Methods Serum samples were collected at 12 h, 24 h, and 72 h after birth in neonates with perinatal asphyxia-induced lung injury. Exosomes were isolated, and the concentration and size distribution were assessed. The exosome surface markers CD9, CD63, CD81, HSP70, and TSG101 were detected by Western blot. The exosome proteins were evaluated by quantitative proteomics using a tandem mass tag (TMT). All the identified proteins were submitted to the Weighted Gene Co-Expression Network Analysis (WGCNA), GO function, and KEGG pathway analysis. A protein-protein interaction network (PPI) was utilized to identify hub proteins with the Cytohubba plugin of Cytoscape.Results The exosomes were round or oval vesicular structures at a diameter range of 100-200 nm, and the size distribution was standard and consistent. Exosome surface markers CD9, CD63, CD81, HSP70, and TSG101 were detected. 444 out of 450 proteins were mapped with gene names. A brown module containing 71 proteins was highly linked with the 12 h phenotype and was predominantly concentrated in lipoprotein and complement activation. The top 10 proteins, APOA1, APOB, APOE, LPA, APOA2, CP, C3, FGB, FGA, and TF, were determined as hub proteins.Conclusion The present study demonstrates comprehensive information for understanding molecular changes of lung injury following perinatal asphyxia, which provides a reliable basis for screening potential biomarkers and therapeutic targets in the clinic.

Abstract Objective To investigate the etiological characteristics of plastic bronchitis (PB) caused by pulmonary infections in children and to identify any differences in the clinical features of PB cases caused by different pathogens. Method We collected data on children diagnosed with PB and admitted to the Respiratory Department at Soochow University Children’s Hospital between July 2021 and March 2023 utilizing electronic bronchoscopy. We analyzed clinical characteristics and the species of pathogens causing the illness in these children. Result A total of 45 children were enrolled. The main clinical symptoms observed were cough (100%), fever (80%), shortness of breath (28.9%), and wheezing (20.0%). Pathogens were identified in 38 (84.4%) patients. Mycoplasma pneumoniae (MP) had the highest detection rate at 53.3%, followed by the Boca virus at 26.7%. MP-induced PB typically occurs in older children with an average age of 7.46 ± 2.36 years, with the main symptoms including high fever (85.7%) and local hyporespiration (42.9%). In contrast, Boca virus-induced PB tends to occur in younger children, with the main symptoms of moderate fever (54.5%), and wheezing (54.5%). The MP group exhibited a higher incidence of both internal and external pulmonary complications, including pleural effusion (42.9%), elevated aspartate aminotransferase (52.4%), lactic dehydrogenase (76.2%), and D-D dimer (90.5%). Conversely, the Boca virus group primarily showed pulmonary imaging of atelectasis (81.8%), with no pleural effusion. The average number of bronchoscopic interventions in the MP group was 2.24 ± 0.62, which was significantly higher than that required in the Boca virus group (1.55 ± 0.52). During the second bronchoscopy, 57.1% of children in the MP group still had visible mucus plugs, while none were observed in the Boca virus group. Conclusion MP and Boca virus are the primary pathogens responsible for PB among children. The clinical manifestations of PB typically vary significantly based on the pathogen causing the condition.

Asthma is an inflammatory disease. Th2 differentiation plays an important role in the pathogenesis of asthma. We explored the role and action mechanism of membrane-associated RING-CH 1 (March1) in the Th2 differentiation regulated by dendritic cells (DCs). Our data showed that the expression of March1 was higher in asthmatic children-derived DCs, asthmatic mice-derived DCs and house dust mites (HDMs)-treated DCs than that in control DCs. Increasing of March1 promoted the production of pro-inflammatory cytokines from HDMs-treated DCs, and enhanced the promotion of HDMs-treated DCs to CD4+T cell proliferation and Th2 differentiation, whereas decreasing of March1 resulted in opposite effects. Furthermore, our data indicated that March1 positively regulated the expression of OX40 ligand (OX40L) and facilitated DCs-induced Th2 differentiation through OX40L. In asthmatic mice, March1-overexpressed DCs significantly aggravated the injury in lung tissues and promoted Th2 differentiation. Overall, our data proved that highly expressed March1 in DCs facilitated asthma development through inducing Th2 differentiation by facilitating OX40L expression. Our data might provide a new idea for the treatment of asthma.

This study aimed to explore the effects of forkhead box P2 gene (Foxp2) on T-helper 9 (Th9) differentiation in asthmatic mice. An in vivo asthmatic mouse model was induced with ovalbumin (OVA). An in vitro model was established by culturing CD4+ T cells with TGF-β, IL-4, and anti-IFN-γ. ELISA, flow cytometry, qRT-PCR and Western blot were performed to examine IL-9 secretion, Th9 cell number, and Th9 cell transcription factor expression, respectively. Pathological changes in lung tissues and airway mucus secretion were assessed with HE and PAS glycogen staining. Anti-IL-9 mAb reversed the elevation in Th9 cells and IL-9 expression in lung tissues and bronchoalveolar lavage fluid (BALF) of asthmatic mice. Foxp2 was downregulated in BALF and lung tissue of asthmatic mice and Th9 cells. Overexpression of Foxp2 inhibited Th9 cell differentiation in vitro and improved airway inflammation in vivo. Our study suggests that overexpression of Foxp2 attenuates allergic asthma by inhibiting Th9 cell differentiation.

The role of micro RNAs (miRNAs) in asthma remains unclear. In this study, we examined the role of miRNA in targeting FOXO1 in asthma. Results showed that miR-493-5p was one of the differentially expressed miRNAs in the PBMCs of asthmatic children, and was also associated with Th cell differentiation. The miR-493-5p expression decreased significantly in the OVA-induced asthma mice than the control groups. The miR-493-5p mimic inhibited the expression of the IL-9, IRF4 and FOXO1, while the inhibitor restored these effects. Moreover, the Dual-Luciferase analysis results showed FOXO1 as a novel valid target of miR-493-5p. According to the rescue experiment, miR-493-5p inhibited Th9 cell differentiation by targeting FOXO1. Then the exosomes in association with the pathogenesis of asthma was identified. Various inflammatory cells implicated in asthmatic processes including B and T lymphocytes, DCs, mast cells, and epithelial cells can release exosomes. Our results demonstrated that the DC-derived exosomes can inhibit Th9 cell differentiation through miR-493-5p, thus DC-derived exosomal miR-493-5p/FOXO1/Th9 may serve as a potential therapeutic target in the development of asthma.

呼吸道感染是儿童时期最常见的感染性疾病,病毒是主要的病原体.新型冠状病毒肺炎(coronavirus disease 2019,COVID-2019)疫情以来,儿童呼吸道病原的流行特征和病原谱均有所变化,病原学检测及持续监测具有重要意义,可为临床诊断、治疗及防控提供依据.