Background:This study aimed to investigate characteristic changes in the upper respiratory tract (URT) microbiome and metabolome in children with asthma and explore their associations with lung function. Methods:Children with asthma aged 6 years and above admitted to the Children's Hospital of Soochow University from December 2022 to December 2023 comprised the study group. Age-matched healthy children undergoing physical examinations in the Department of Child Health were recruited as controls. Throat swabs were collected for microbiome detection using 16S rDNA sequencing and metabolomics analysis using liquid chromatography-mass spectrometry (LC-MS). Results:(1) Significant differences in alpha and beta diversity were observed among the control group (H), chronic persistent asthma group (CA), and acute exacerbation group (AA). In both CA and AA groups, FVC% predicted (FVC%/Pred) and FEV1% predicted (FEV1%/Pred) were negatively correlated with URT microbiota abundance. Actinobacillus abundance was positively correlated with FEV1%/Pred, FEV1/FVC, FEF25%/Pred, FEF50%/Pred, and FEF75%/Pred. (2) Metabolite differences between CA and AA groups were analyzed, and the top 5 differential metabolites were evaluated for their accuracy as asthma assessment biomarkers. L-carnitine showed an AUC > 0.9, with a sensitivity of 85.7% and specificity of 85%. Other differential metabolites, including monoisobutyl phthalate, 4-hexyl-2,5-dimethyloxazole, and dibutyl phthalate, correlated with several lung function indices. The most relevant differential metabolic pathways included arginine biosynthesis, alanine-aspartate-glutamate metabolism, central carbon metabolism in cancer, and D-amino acid metabolism. Conclusion:The URT microbiota in asthmatic children exhibits alterations in composition, structure, and diversity, with lower diversity in acute asthma compared to chronic persistent asthma. At the genus level, some microbiota (Actinobacillus, Fusobacterium) were correlated with FEV1%/Pred, FEV1/FVC, FEF25%/Pred, FEF50%/Pred, FEF75%/Pred. The differential metabolite L-carnitine may be a potential biomarker for asthma assessment.

Background This study aims to evaluate the incidence and risk factors for cytomegalovirus (CMV) DNAemia and its association with disease severity in infants with community-acquired pneumonia (CAP) complicated by respiratory syncytial virus (RSV) infection. Methods In this retrospective, cross-sectional study, we investigated the clinical characteristics of consecutive infants diagnosed with CAP complicated with RSV infection and circulatory whole blood CMV DNA on admission. Using binary logistic regression analysis, the clinical data of these infants were analyzed to identify risk factors for disease severity and CMV DNAemia. Results In all, 241 infants with CAP complicated by RSV infection were enrolled in this study. Fifty-five (22.8%) of these infants had CMV DNAemia. Disease severity was greater in infants with CMV DNAemia than in those without. Additionally, CMV DNAemia (odds ratio [OR], 5.517; 95% confidence interval [CI], 1.839–16.553; P = 0.002) was found to be an independent risk factor for pediatric intensive care unit admission. Furthermore, age (+ 1 month; OR, 0.772; 95% CI, 0.617–0.965; P = 0.023), possible bacterial coinfection (OR, 2.392; 95% CI, 1.115–5.121; P = 0.025), and peripheral leukocyte count (+ 1 × 109/L; OR, 1.220; 95% CI, 1.093–1.362; P < 0.001) were independent risk factors for CMV DNAemia. Conclusions Young age, possible bacterial coinfection, and higher peripheral leukocyte count were associated with an increased risk of CMV DNAemia, while infants with CMV DNAemia had greater disease severity than those without. Clinical trial number: Not applicab

Mycoplasma pneumoniae pneumonia (MPP) is a common pediatric respiratory infection linked to excessive immune-inflammatory responses. This study investigated the role of the Notch ligand DLL4 in the immunopathogenesis of MPP by assessing its expression in peripheral blood mononuclear cells of affected children. A total of 128 children with MPP and 35 controls were recruited. PBMCs were analyzed for the expression of Notch ligands (Jagged1, Jagged2, DLL1, DLL4) using real-time PCR. Lymphocyte subsets were assessed via flow cytometry, and cytokine levels were measured using ELISA. Clinical data were compared between severe and mild MPP cases, and correlations between DLL4 expression and immune indicators were evaluated. DLL4 expression was significantly higher in the MPP and severe MPP groups than in controls (P < 0.01). MPP patients showed lower CD3+ and CD3+CD4+ lymphocyte levels, and higher CD3+CD8+ and CD3-CD19+ levels compared with controls (P < 0.001). Plasma levels of IFN-γ, IL-17, and IL-36α were elevated in MPP patients (P < 0.001), whereas IL-4 and IL-10 levels were reduced (P < 0.01). Severe cases had higher IFN-γ, IL-17, and IL-36α levels than mild cases (P < 0.05). DLL4 expression positively correlated with plasma IFN-γ and IL-17 levels in MPP patients (P < 0.05). Elevated DLL4 expression in MPP patients, particularly in severe cases, suggests its role in enhancing Th1/Th17-mediated immune responses while suppressing Th2 pathways. Such findings implicate the Notch signaling pathway, via DLL4, in the immunopathogenesis of MPP and highlight its potential as a therapeutic target for modulating immune responses in severe MPP.

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 examine chemokine expression in children with Respiratory Syncytial Virus (RSV) bronchiolitis and evaluate its clinical utility for early warning and prognosis. Five hospitalised RSV bronchiolitis children and five matched controls were studied. To validate findings, 50 RSV infants and 30 controls were assessed for recurrent wheezing after 1 year. Blood leukocyte RNA-seq identified RSV-associated hub genes via GO/KEGG analysis, with flow cytometry confirming chemokine expression. Twelve hub genes were identified, with 712 differentially expressed genes (292 upregulated, 420 downregulated). RSV patients showed elevated CXCL2, CXCL12, CXCL13, CCL13, and CCL24 (P < 0.05). CXCL12 was higher in moderate-to-severe cases (Area Under the Curve, AUC = 0.835, 95% CI 0.714-0.956, P < 0.05), while CXCL13 was elevated in recurrent wheezers (AUC = 0.851, 95% CI 0.711-0.991, P < 0.05). CXCL12 predicted severity, and CXCL13 predicted recurrence (ROC-confirmed, P < 0.05). CXCL12 and CXCL13 may serve as biomarkers for assessing RSV bronchiolitis severity and predicting recurrence, aiding early clinical evaluation and prognosis.

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

Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease in preterm infants, characterized by dysregulated macrophage polarization and oxidative stress. While mesenchymal stem cell-derived exosomes (MSC-Exos) have shown protective effects against BPD, the role of exosomes derived from hypoxia-preconditioned MSCs (Hypo-Exos) remains unclear. This study aimed to investigate whether Hypo-Exos alleviate BPD by modulating alveolar macrophage (AM) polarization and oxidative stress via the mitochondrial transporter SLC25A3. We utilized in vitro models of LPS-induced M1 polarization and H2O2-induced oxidative stress in AMs, as well as an in vivo rat model of BPD induced by intermittent hypoxia. Our data demonstrate that hypoxic preconditioning enhanced exosome secretion from MSCs. Furthermore, hypoxic preconditioning promoted the packaging of SLC25A3 into these exosomes. Hypo-Exos significantly suppressed M1 polarization, reduced oxidative stress, and ameliorated lung injury and dysfunction in BPD rats. Silencing SLC25A3 in MSCs abolished these protective effects. Mechanistically, SLC25A3 interacted with PTEN, leading to inhibition of PTEN expression and activation of the PI3K/AKT signaling pathway. Overexpression of PTEN reversed the beneficial effects of SLC25A3 on macrophage polarization and oxidative stress. These findings reveal that Hypo-Exos deliver SLC25A3 to AMs, thereby downregulating PTEN, activating PI3K/AKT signaling, promoting M2 polarization, attenuating oxidative damage, and ultimately mitigating BPD progression. This study provides important mechanistic insights and suggests potential therapeutic avenues for exosome-based treatment of BPD.

Kawasaki disease (KD), characterized by systematic vasculitis, is a leading cause of pediatric heart disease. Although recent studies have highlighted the critical role of deubiquitinases in vascular pathophysiology, their specific contribution to KD remains largely unknown. Herein, we investigated the function of the deubiquitinase USP7 in both KD patients and a CAWS-induced KD murine model. USP7 expression level is increased both in HCAECs induced by KD sera and cardiac CD31+ endothelial cells of KD mice. Whereas knockout of USP7 increases the cellular proportion of endothelial cells and potentially attenuates the elevated EndoMT, fibrosis, and inflammation in cardiac tissue of KD mice, consistently with the in vitro experiment observed in HCAECs induced by TGF-β2. Mechanistically, USP7 interacts with SMAD2/3, enhancing their protein stability by removing the K48 ubiquitin chain from both proteins and preventing their proteasome degradation, thus increasing the p-SMAD2 levels and nuclear entry. Importantly, intraperitoneal injection of USP7 inhibitor, P22077 elicited a robust anti-EndoMT and anti-vascular inflammation effect in KD model mice. Therefore, our study uncovered a previously unrecognized function of increased USP7 in KD by augmenting TGFβ2/SMAD2/SMAD3 signaling, thus facilitating the transcription of genes implicated in the EndoMT, cardiac fibrosis, and vascular remodeling. Our finding suggests that USP7 could serve as a potential therapeutic target for the prevention and treatment of coronary artery lesions in KD and related vascular diseases.

Background:The outbreak of coronavirus disease 2019(COVID-19)infection posed a huge threat and bur-den to public healthcare in late 2022.Non-drug measures of traditional Chinese medicine(TCM),such as acupuncture,cupping and moxibustion,are commonly used as adjuncts in China to help in severe cases,but their effects remain unclear. Objectives:To observe the clinical effect of TCM non-drug measures in improving respiratory function and symptoms among patients with severe COVID-19. Design,setting,participants and interventions:This study was designed as a multicenter,assessor-blind,randomized controlled trial.Hospitalized patients with COVID-19 were randomly assigned to the treat-ment or control group.The treatment group received individualized TCM non-drug measures in combi-nation with prone position ventilation,while the control group received prone position ventilation only for 5 consecutive days. Main outcome measures:The primary outcome measures were the percentage of patients with improved oxygen saturation(SpO2)at the end of the 5-day intervention,as well as changes of patients'respiratory rates.The secondary outcome measures included changes in SpO2 and total score on the self-made res-piratory symptom scale.The improvement rate,defined as a 3-day consecutive increase in SpO2,the duration of prone positioning,and adverse events were recorded as well. Results:Among the 198 patients included in the intention-to-treat analysis,159(80.3％)completed all assessments on day 5,and 39(19.7％)patients withdrew from the study.At the end of the intervention,71(91％)patients in the treatment group had SpO2 above 93％,while 61(75.3％)in the control group reached this level.The proportion of participant with improved SpO2 was significantly greater in the intervention group(mean difference[MD]=15.7;95％confidence interval[CI]:4.4,27.1;P=0.008). Compared to the baseline,with daily treatment there were significant daily decreases in respiratory rates in both groups,but no statistical differences between groups were found(all P ≥ 0.05).Compared to the control group,the respiratory-related symptoms score was lower among patients in the treatment group(MD=-1.7;95％CI:-2.8,-0.5;P=0.008)after day 3 of treatment.A gradual decrease in the total scores of both groups was also observed.Thirty-one adverse events occurred during the intervention,and 2 patients were transferred to the intensive care unit due to deterioration of their illness. Conclusion:TCM non-drug measures combined with prone positioning can effectively treat patients with severe COVID-19.The combined therapy significantly increased SpO2 and improved symptom scores compared to prone positioning alone,thus improving the patients'respiratory function to help them recover.However,the improvement rate did not differ between the two groups.

BackgroundThis study aimed to investigate the clinical characteristics of pediatric patients hospitalized with community-acquired pneumonia (CAP) and concomitant cytomegalovirus (CMV) infection.MethodsThis cross-sectional study enrolled consecutive pediatric patients admitted with CAP who tested positive for CMV DNA in bronchoalveolar lavage fluid (BALF). Flexible fiberoptic bronchoscopy was performed when routine treatment for CAP proved ineffective. The study participants were further stratified into two groups based on CMV serological test results: recent CMV infection group and CMV replication group. Clinical characteristics were compared between these two groups.ResultsAmong 124 patients aged 1–11 months included in this study, 80 (64.5%) patients were categorized as having recent CMV infection, and 44 (35.5%) tested positive for CMV replication. Co-infection with other pathogens was detected more frequently in the CMV replication group (n = 29, 65.9%) than in the recent CMV infection group (n = 35, 43.7%; P = 0.018). Patients with recent CMV infection were younger and exhibited higher levels of alanine transaminase (ALT) and aspartate aminotransferase compared to those with CMV replication (all P < 0.05). Multivariable regression analysis showed age was independently associated with recent CMV infection (odds ratio [OR], 0.707; 95% confidence interval [CI], 0.586–0.853; P < 0.001). Notably, receiver operating characteristic curve analysis showed that a CMV PCR level of 3,840 copies/ml in blood samples had a sensitivity of 34.7% and specificity of 90.0% for diagnosis of recent CMV infection with an area under the curve (AUC) of 0.625 (95% CI: 0.513–0.736, P = 0.048). A CMV PCR level of 6,375 copies/ml in urine samples had a sensitivity of 77.1% and specificity of 61.5% for diagnosis of recent CMV infection with an AUC of 0.695 (95% CI: 0.531–0.858, P = 0.04). Furthermore, multivariate linear regression analysis revealed that the blood CMV DNA copy number was associated with ALT (B = 0.001; P < 0.001).ConclusionsThe CMV DNA copy numbers in blood and urine could serve as discriminatory markers between recent CMV infection and CMV replication. Measuring CMV DNA levels in blood may be an effective method for monitoring liver function impairment in pediatric patients presenting with CAP and concurrent CMV infection.

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.

Objective: To investigate the significance of VISTA in bronchial asthma and its impact on the disease. Methods: Human peripheral blood of asthma children was gathered. The expression concentrations of VISTA, IL-4, IL-6, CD25, CD40L, and PD-L2 in peripheral blood plasma were detected by ELISA. We established the mouse model of asthma and intervened with agonistic anti-VISTA mAb (4C11) and VISTA fusion protein. ELISA, flow cytometry, and Western blotting were performed to detect the expression levels of Th1, Th2, and Th17 cell subsets and related characteristic cytokines, as well as the protein levels of MAPKs, NF-kappa B, and TRAF6 in lung tissues. In addition, the infiltration of eosinophils and inflammatory cells, airway mucus secretion, and VISTA protein expression in lung histopathological sections of different groups of mice were analyzed. Results: The concentration of VISTA in human asthma group decreased significantly (p < 0.05); A positive correlation was observed between VISTA and CD40L. The intervention of 4C11 mAb and fusion protein respectively during the induction period increase the differentiation of Th1 cells and the secretion of IFN-gamma, and inhibit the differentiation of Th2 and Th17 cells, as well as the secretion of IL-4, IL-5, IL-13 and IL-17, partially reduce the pathological changes of asthma in mouse lungs and correct the progress of asthma. The MAPK, NF-kappa B, and TRAF6 protein levels were the middle range in the 4C11 mAb and fusion protein groups (p < 0.05). Conclusion: The findings suggest VISTA may play a negative regulatory role in the occurrence and development of bronchial asthma.

Background:This study aimed to analyze the clinical features of children with lobar pneumonia caused by Mycoplasma pneumoniae (MP) infection, to explore the independent risk factors for bronchoscopic intervention in children with lobar pneumonia caused by MP infection. There is a lack of objective assessment tools to guide the use of bronchoscopy in clinical practice. For children with lobar pneumonia caused by MP infection, whether line shall be actively bronchoscope intervention therapy remains to be further defined. We also aimed to construct an early warning model of bronchoscopic intervention to provide an objective evaluation tool for clinicians. Methods:We collected the clinical data of 533 children with lobar pneumonia caused by MP infection. The patients were divided into three groups according to the interventional indications for bronchoscopy and whether they were treated with bronchoscopic intervention, and the clinical features and prognosis of the three groups were compared. A binary logistic regression analysis was performed on the indicators with a significance value of P<0.05, which we retrieved from the comparative analysis between the first two groups to uncover the independent risk factors and regression equations concerning bronchoscopic intervention. The regression coefficient (β) of our regression model was then used to score related values in the model to construct a predictive scoring model of bronchoscopic intervention for the treatment of children with lobar pneumonia caused by MP infection. Results:Children with lobar pneumonia caused by MP infection who demonstrated absolute indications for bronchoscopy exhibited more severe clinical manifestations, and children without absolute indications for bronchoscopy had a better prognosis even without bronchoscopic intervention. To establish our early warning model of bronchoscopic intervention for children with lobar pneumonia caused by MP infection, we used the following indices: C-reactive protein ≥20.94 mg/L (β1=2.253) received 3 points, while a fever duration before bronchoscopy ≥6.5 d (β2=1.424), lactate dehydrogenase ≥461.5 U/L (β3=1.246), or fever (β4=1.223) each received 2 points, and the complication of pleural effusion (β5=0.841) received 1 point, for a total possible score of 10 points. Conclusions:When the score for the children with lobar pneumonia caused by MP infection was ≥6, the possibility of bronchoscopic intervention for treatment was >80%. The higher the score, the greater the possibility of bronchoscopic intervention.

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.

Neonatal meningitis is rare but devastating disease. Multidrug-resistant (MDR, multi-drug resistant) bacteria are a major global health risk. We report an Escherichia coli meningitis isolate with multiple resistance patterns and unusual serotype (O75) that caused sudden neonatal death. The isolate was resistant to antibiotics other than cefoperazone/sulbactam and imipenem, challenging the combination of antibiotics commonly used in the empirical treatment of neonatal sepsis. Despite aggressive symptomatic and supportive treatment of the infant based on laboratory tests and clinical practice, the infant eventually died. This is the first case of meningoencephalitis due to serotype O75 reported in China. The presence of highly pathogenic multidrug-resistant microorganisms isolated in neonates underscores the need to implement rapid resistance diagnostic methods and should prompt consideration of alternatives to empiric treatment of neonatal bacterial meningitis.

BackgroundPredicting intravenous immunoglobulin (IVIG)-resistant Kawasaki disease (KD) can aid early treatment and prevent coronary artery lesions. A clinically consistent predictive model was developed for IVIG resistance in KD.MethodsIn this retrospective cohort study of children diagnosed with KD from January 1, 2016 to December 31, 2021, a scoring system was constructed. A prospective model validation was performed using the dataset of children with KD diagnosed from January 1 to June 2022. The least absolute shrinkage and selection operator (LASSO) regression analysis optimally selected baseline variables. Multivariate logistic regression incorporated predictors from the LASSO regression analysis to construct the model. Using selected variables, a nomogram was developed. The calibration plot, area under the receiver operating characteristic curve (AUC), and clinical impact curve (CIC) were used to evaluate model performance.ResultsOf 1975, 1,259 children (1,177 IVIG-sensitive and 82 IVIG-resistant KD) were included in the training set. Lymphocyte percentage; C-reactive protein/albumin ratio (CAR); and aspartate aminotransferase, sodium, and total bilirubin levels, were risk factors for IVIG resistance. The training set AUC was 0.825 (sensitivity, 0.723; specificity, 0.744). CIC indicated good clinical application of the nomogram.ConclusionThe nomogram can well predict IVIG resistance in KD. CAR was an important marker in predicting IVIG resistance in Kawasaki disease.

Abstract Background This study aimed to investigate the clinical significance of detecting cytomegalovirus (CMV) in the blood and urine of pediatric patients hospitalized with community-acquired pneumonia (CAP) and CMV infection. Methods This retrospective case-control study enrolled consecutive pediatric patients admitted with CAP with a positive test result for CMV DNA in bronchoalveolar lavage fluid (BALF). The study participants were further divided into two groups based on CMV serological test results: active CMV infection group and CMV replication group. Clinical characteristics were compared between these two groups. The Kruskal–Wallis test or Mann–Whitney U test was used to compare non-normally distributed continuous variables. The Chi-squared test was used to assess differences in categorical variables. The correlations between CMV copy number and ALT were determined using the Spearman correlation analysis. Results Among 124 patients aged 1–11 months included in this study, 80 (64.5%) patients were categorized as having an active CMV infection and 44 (35.5%) as positive for CMV replication. Co-infection with other pathogens was detected more frequently with CMV replication (n = 29, 65.9%) compared with active CMV infection (n = 35, 43.7%; P = 0.018). Patients with active CMV infection were younger and exhibited higher levels of alanine transaminase (ALT) and aspartate aminotransferase compared with patients with CMV replication (all P < 0.05). The median CMV DNA copy numbers in both blood and urine were higher in patients with active CMV infection than in patients with CMV replication (all P < 0.05). Both the blood and urine CMV DNA copy numbers showed a positive association with ALT (r = 0.237, P = 0.017 for blood and r = 0.309, P = 0.033 for urine). Conclusions Measurement of CMV DNA in blood and urine may be an effective method for monitoring liver function impairment in patients presenting with CAP and concurrent CMV infection.

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.

Background: Kawasaki disease (KD) is a systemic vasculitis that commonly affects children and its etiology remains unknown. Growing evidence suggests that immune-mediated inflammation and immune cells in the peripheral blood play crucial roles in the pathophysiology of KD. The objective of this research was to find important biomarkers and immune-related mechanisms implicated in KD, along with their correlation with immune cells in the peripheral blood. Material/Methods: Gene microarray data from the Gene Expression Omnibus (GEO) was utilized in this study. Three datasets, namely GSE63881 (341 samples), GSE73463 (233 samples), and GSE73461 (279 samples), were obtained. To find intersecting genes, we employed differentially expressed genes (DEGs) analysis and weighted gene co-expression network analysis (WGCNA). Subsequently, functional annotation, construction of protein-protein interaction (PPI) networks, and Least Absolute Shrinkage and Selection Operator (LASSO) regression were performed to identify hub genes. The accuracy of these hub genes in identifying KD was evaluated using the receiver operating characteristic curve (ROC). Furthermore, Gene Set Variation Analysis (GSVA) was employed to explore the composition of circulating immune cells within the assessed datasets and their relationship with the hub gene markers. Results: WGCNA yielded eight co-expression modules, with one hub module (MEblue module) exhibiting the strongest association with acute KD. 425 distinct genes were identified. Integrating WGCNA and DEGs yielded a total of 277 intersecting genes. By conducting LASSO analysis, five hub genes (S100A12, MMP9, TLR2, NLRC4 and ARG1) were identified as potential biomarkers for KD. The diagnostic value of these five hub genes was demonstrated through ROC curve analysis, indicating their high accuracy in diagnosing KD. Analysis of the circulating immune cell composition within the assessed datasets revealed a significant association between KD and various immune cell types, including activated dendritic cells, neutrophils, immature dendritic cells, macrophages, and activated CD8 T cells. Importantly, all five hub genes exhibited strong correlations with immune cells. Conclusion: Activated dendritic cells, neutrophils, and macrophages were closely associated with the pathogenesis of KD. Furthermore, the hub genes (S100A12, MMP9, TLR2, NLRC4, and ARG1) are likely to participate in the pathogenic mechanisms of KD through immune-related signaling pathways.

ObjectiveClimate and environmental change is a well-known factor causing bronchial asthma in children. After the outbreak of coronavirus disease (COVID-19), climate and environmental changes have occurred. The present study investigated the relationship between climate changes (meteorological and environmental factors) and the number of hospitalizations for pediatric bronchial asthma in Suzhou before and after the COVID-19 pandemic.MethodsFrom 2017 to 2021, data on daily inpatients diagnosed with bronchial asthma at Children's Hospital of Soochow University were collected. Suzhou Meteorological and Environmental Protection Bureau provided daily meteorological and environmental data. To assess the relationship between bronchial asthma-related hospitalizations and meteorological and environmental factors, partial correlation and multiple stepwise regression analyses were used. To estimate the effects of meteorological and environmental variables on the development of bronchial asthma in children, the autoregressive integrated moving average (ARIMA) model was used.ResultsAfter the COVID-19 outbreak, both the rate of acute exacerbation of bronchial asthma and the infection rate of pathogenic respiratory syncytial virus decreased, whereas the proportion of school-aged children and the infection rate of human rhinovirus increased. After the pandemic, the incidence of an acute asthma attack was negatively correlated with monthly mean temperature and positively correlated with PM2.5. Stepwise regression analysis showed that monthly mean temperature and O3 were independent covariates (risk factors) for the rate of acute asthma exacerbations. The ARIMA (1, 0, 0) (0, 0, 0) 12 model can be used to predict temperature changes associated with bronchial asthma.ConclusionMeteorological and environmental factors are related to bronchial asthma development in children. The influence of meteorological and environmental factors on bronchial asthma may be helpful in predicting the incidence and attack rates.