Childhood obesity-related asthma is a distinct and increasingly prevalent phenotype, associated with greater symptom burden, poorer disease control, frequent exacerbations, and reduced responsiveness to standard therapy. This phenotype is complex and heterogeneous, with underlying mechanisms involving airway inflammation, adipokine imbalance, metabolic dysregulation, changes in the gut microbiome, and altered respiratory mechanics. Current treatment for these children remains challenging, as they often show reduced responsiveness to standard inhaled corticosteroids. Multidisciplinary strategies including weight reduction, lifestyle interventions, and careful management of comorbidities are therefore essential. Emerging evidence suggests potential roles for metabolic drugs, biologic therapies, and microbiota-targeted interventions, although pediatric-specific data are still limited. Therefore, in this review, we summarize the epidemiology, pathogenesis, clinical features, and management of obesity-related asthma in children. We also highlight important gaps in knowledge and emphasize the need for large-scale, pediatric-focused, multicenter studies to develop effective, phenotype-specific treatment strategies for this growing and vulnerable patient population.
Background:Mucoid sputum is common in pediatric patients with lower respiratory tract infection (LRTI) and can exacerbate cough, contribute to difficulty in expectoration and dyspnea, and even cause suffocation. Although ambroxol hydrochloride and clenbuterol hydrochloride oral solution [AHCHOS (or Yitanjing)] is widely used in pediatric practice, high-quality real-world evidence comparing it with conventional expectorant therapies such as ambroxol hydrochloride injection (AHI) remains limited. This study aimed to investigate the efficacy and safety of AHCHOS in pediatric patients with LRTI complicated with mucoid sputum. Methods:This multicenter, non-randomized observational study included 407 hospitalized pediatric patients with LRTI complicated by mucoid sputum across 30 institutions in China. Patients received AHCHOS (n=254) or AHI (n=153) based on clinical judgment and guardian preference. Inclusion criteria comprised age ≤14 years, confirmed LRTI diagnosis, and clinically significant sputum symptoms. Respiratory symptoms were assessed using a composite symptom score and a visual analog scale (VAS) at baseline and Day 7. Safety was evaluated through routine clinical monitoring, including vital signs, physical examination, and laboratory assessments. Results:The baseline features, including family history of respiratory disease (P<0.001) and type of the episode (P=0.02), differed between groups. The decline in total respiratory symptom score was greater in the AHCHOS group than in the AHI group at D7 (-4.35±2.25 vs. -3.56±1.89; P<0.001), as was the decrease in corresponding percentage (-77%±30% vs. -65%±28%; P<0.001). Regarding subscales, the decrease in cough (P<0.001), sputum amount (P=0.03), and wheezing rale (P=0.008) scores was significantly greater in the AHCHOS group than in the AHI group at D7, but the expectoration difficulty score was not (P=0.90). Meanwhile, the decrease in VAS score for self-reported symptom severity was greater in the AHCHOS group than in the AHI group at D7 (-4.12±2.04 vs. -3.51±1.78; P=0.006). Moreover, no adverse reactions were reported in either group. Conclusions:AHCHOS was associated with improved respiratory symptom outcomes and was well tolerated in pediatric patients with LRTI complicated by mucoid sputum.
Blomia tropicalis is a clinically significant source of mite allergens, with Blo t 5 identified as a major component. This study aimed to produce recombinant Blo t 5 (rBlo t 5) and investigate its role in allergic immune responses. The rBlo t 5 protein (∼14 kDa) was successfully expressed in E. coli and purified with high purity. IgE-ELISA demonstrated specific IgE binding in 69% of serum samples from asthmatic children sensitized to B. tropicalis. Transcriptomic analysis of rBlo t 5-stimulated BEAS-2B bronchial epithelial cells revealed significant enrichment of genes associated with the interleukin-10 signaling and DDX58/IFIH1-mediated interferon-alpha/beta pathways. qPCR validation confirmed upregulation of key genes, including of CXCL1, CXCL2, CCL2, CCL5, IL1B, ICAM-1, RIG-I, IFIH1, IRF7, and ISG15. In a murine model of allergic airway inflammation, rBlo t 5 sensitization induced pronounced inflammatory cell infiltration, goblet cell hyperplasia, collagen deposition, and increased neutrophils in bronchoalveolar lavage fluid. Serum levels of allergen-specific IgE and IgG1 were elevated, accompanied by a Th2-skewed cytokine profile (increased IL-4 and IL-13, decreased IFN-γ and TGF-β). qPCR of lung tissues further confirmed upregulation of the same pathway-related genes.These findings indicate that rBlo t 5 elicits a type 2-polarized immune response initiated, in part, through the concurrent activation of the IL-10 and DDX58/IFIH1-interferon signaling axes in airway epithelium, providing new mechanistic insights into B. tropicalis-induced allergic inflammation.
IntroductionCarbapenem-resistant Enterobacteriaceae (CRE) is the most common clinical pathogens. Investigating the antimicrobial resistance, hypervirulence and clinical characteristics of CRE isolated from children is helpful to guide for anti-infection treatments.MethodsNonduplicated CRE clinical strains were isolated and mass spectrometry was applied to identify clinical isolated strains. VITEK 2 Compact system and Kirby-Bauer method were used to analyze the antimicrobial susceptibility. Besides, the drug resistance and hypervirulence associated genes were detected by polymerase chain reaction (PCR) and sequencing.ResultsA total of 281 non-duplicated CRE strains were identified in this study. Klebsiella pneumoniae (55.87%), Escherichia coli (36.65%) and Klebsiella aerogenes (3.20%) were the top 3 CRE strains. These strains showed high resistance to most of antimicrobial agents and carried carbapenemase genes, including blaOXA-232 (38.08%), blaKPC-2 (20.28%), blaOXA-1 (17.08%), blaNDM-5 (10.32%) and blaNDM-1 (8.90%). In addition, blaTEM-1 (98.93%), blaCTX-M-14 (88.61%) and blaSHV-11 (87.54%) were the prevalent extended-spectrum β-lactamase (ESBL) genes in these strains, while the detection rate of AmpC cephalosporinase genes were not high. Besides, 45 (28.66%) carbapenem-resistant Klebsiella pneumoniae (CRKP) strains carried hypervirulence associated genes iucA (24.84%), prmpA (17.83%), peg-344 (17.20%), and prmpA2 (9.55%). Among them, 22 (14.01%) CRKP strains were also identified as carbapenem-resistant and hypervirulent Klebsiella pneumoniae (CR-HVKP). What’s worse, the patients infected with CR-HVKP had a worse prognosis overall.ConclusionThis study revealed the drug resistance, hypervirulence and epidemiology of CRE strains in pediatric patients in Suzhou of eastern China. Unfortunately, CR-HVKP strains with more several infection were also identified, which should be of great concern to clinicians.
The trends in allergic comorbidities secondary to the environmental variations in China remain unclear. We aimed to determine the variation of allergic comorbidities and polysensitization among asthma and/or rhinitis patients in the past decade. We assessed two nationally representative cross-sectional datasets from 2008 to 2009 and 2018 to 2019, which enrolled 2322 and 2353 patients, respectively. Over the present 10-year study period, the prevalence of allergic symptoms and allergen sensitivity among patients with multiple sensitivities in the 2018-2019 cohort was significantly higher than that in the 2008-2009 cohort, especially for mites, pollen, and animal allergens. The comorbidity rates of asthma, allergic rhinitis, conjunctivitis, and eczema were significantly increased in the 2018-2019 cohort. Also in that cohort, IgE polysensitization was significantly associated with the coexistence of asthma and rhinitis, and the number of IgE-reactive allergens was significantly associated with the number of multimorbidities. Use of an air-conditioner and carpet in the home, and keeping pet were linked to the risk of polysensitization. Our findings suggest an increase in the comorbidity rate and multimorbid polysensitized phenotype of allergic diseases in China. Asthma occurred in both cohorts more frequently with coexisting allergies than as a single entity.
Glycosylation is a critical post-translational modification that regulates protein folding, stability, and cellular communication. Among glycan modifications, fucosylation, catalyzed by fucosyltransferases (FUTs), plays important roles in immune regulation, epithelial homeostasis, and host-pathogen interactions. Increasing evidence suggests that dysregulated fucosylation contributes to chronic inflammatory airway diseases, including asthma. Asthma is characterized by chronic airway inflammation, epithelial barrier dysfunction, mucus hypersecretion, and airway remodeling, processes that are increasingly associated with altered glycosylation patterns. Recent studies indicate that specific FUT isoforms regulate epithelial integrity, mucin glycosylation, immune-cell recruitment, and inflammatory signaling in asthma. Emerging evidence also suggests that FUT-mediated fucosylation may contribute to airway remodeling and cellular senescence; however, direct evidence for these mechanisms in asthma remains limited, and many insights are derived from related respiratory diseases and experimental models. This review summarizes current knowledge of the FUT family and critically evaluates the evidence linking aberrant fucosylation to asthma pathogenesis. We discuss the roles of FUTs in epithelial dysfunction, mucus secretion, immune regulation, airway remodeling, and cellular senescence, while distinguishing established asthma-specific findings from emerging mechanistic hypotheses. Finally, we highlight current challenges, future research directions, and the potential of FUT-targeted strategies for biomarker discovery and precision therapies in asthma.
Objective Ambroxol hydrochloride and clenbuterol hydrochloride oral solution (AHCHOS) is an agent with mucolytic and bronchodilator functions, but its clinical application in child patients with lower respiratory tract infections (LRTI) and symptoms of mucoid sputum needs more investigation. This study aimed to investigate efficacy of AHCHOS, its influencing factors, and effect on quality of life in these patients. Methods This study enrolled 254 hospitalized child patients with LRTI and symptoms of mucoid sputum receiving AHCHOS. Results Total cough of respiratory symptom (QS) score and QS scores of each subscale (cough, amount of sputum, difficulty in expectoration, and wheeling rale) on the 7th day (D7) were decreased than those at baseline (all P < 0.001). After multivariate logistic regression analysis, non parental guardian status (OR = 25.641, P = 0.020), respiratory rate (OR = 1.075, P = 0.019), and neutrophil percentage (OR = 1.034, P = 0.026) were independently related to higher possibility of absolute value of change of total QS score>5. Quality of life visual analog scale score on D7 was reduced than that at baseline (P < 0.001). Medication compliance was 98.00% on the 4th day, 92.68% on D7, 76.00% on the 14th day, and 75.95% on the 28th day. No adverse event occurred. Conclusion AHCHOS alleviates respiratory symptoms and improves quality of life with good safety in child patients with LRTI and symptoms of mucoid sputum, which is more beneficial for those with elevated respiratory rate, higher neutrophil percentage, and nonparental guardians.
Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in children. Among viral components, the M2-1 protein is essential for efficient transcription and replication. Given its pivotal role in the viral life cycle, host factors that regulate this process may represent potential therapeutic targets against RSV. In this study, we identified the E3 ubiquitin ligase ZFP91 as a host factor that restricts RSV replication. Notably, RSV infection upregulated ZFP91 expression; ZFP91 overexpression significantly suppressed viral replication, whereas ZFP91 knockdown increased viral titers and viral gene expression, including that of M2-1 and N. Importantly, in an RSV-infected mouse model, epithelial-specific loss of ZFP91 increased viral burden and M2-1 protein levels in lung tissues, confirming its antiviral function in vivo. Mechanistically, ZFP91 directly interacted with M2-1 and promoted its degradation by catalyzing K48-linked polyubiquitination at lysine residues 8, 48, and 52. Collectively, these findings identify ZFP91 as a key regulator of RSV replication and reveal a novel antiviral mechanism mediated by its E3 ubiquitin ligase activity. This work thus provides new insights into RSV pathogenesis and host–virus interactions.
Purpose:To evaluate the association of ambroxol hydrochloride and clenbuterol hydrochloride oral solution (AHCHOS) with respiratory symptom improvement and safety in Chinese children with pneumonia using real-world data. Methods:A propensity score-matched (PSM) cohort study was conducted. Children patients (≤14 years) with a diagnosis of pneumonia between May, 2018 and July, 2019 were considered as the study population. The main outcome of interest was the overall rate of improvement of respiratory symptoms in treatment groups with or without AHCHOS at day 7 using respiratory symptom scores (QS) and Visual Analog Scale (VAS) score of severity of respiratory signs. Secondary end points include medication adherence assessment and safety assessment. Results:A total of 3103 children with a diagnosis of pneumonia were included. After propensity score matching, a sample of 1428 patients was analyzed. AHCHOS use was associated with greater improvement in cough score (p=0.01) and day 7 clinical sign improvement rate (p=0.03) compared with no AHCHOS use. Exploratory subgroup analyses suggested larger differences in children aged 3-6 years and in selected severity strata. Medication adherence assessmentdid not differ significantly between groups at days 4, 7, 14, and 28. Adverse events were similar between groups. Conclusion:In this real-world propensity score-matched analysis, AHCHOS use was associated with improved respiratory symptom outcomes in children with pneumonia and appeared to have an acceptable safety profile. These findings should be interpreted as observational and hypothesis-generating. Trial Registration Number:The study was registered at Chinese Clinical Trial Registry (https://www.chictr.org.cn/, ChiCTR1800015818).
Type I interferons (IFN-I) are essential for antiviral immunity, and precise regulation of IFN-I production is crucial to balance viral clearance and immunopathology. Here, we demonstrate that the interferon-stimulated gene TOR3A negatively regulates type I IFN signalling during respiratory syncytial virus (RSV) infection. TOR3A expression was upregulated in macrophages and RSV-infected patients, and its deficiency enhanced antiviral responses, leading to reduced viral load. Mechanistically, RSV infection induced TOR3A expression through the IFN-STAT1 pathway, which in turn suppressed IFN-I production. Furthermore, TOR3A recruited the E3 ubiquitin ligase STUB1 to mediate K48-linked ubiquitination and proteasomal degradation of RIG-I at lysine 146, thereby promoting RSV immune evasion. Our study identifies TOR3A as a novel suppressor of antiviral immunity and uncovers a mechanism by which RSV exploits host ISGs to dampen IFN-I responses, providing new insights into viral pathogenesis and potential therapeutic strategies.
Proteins containing the broad-complex, tramtrack and bric-à-brac (BTB) domain, also referred to as the poxvirus and zinc finger (POZ) domain, play a variety of cellular roles. As key mediators of protein-protein interactions, these proteins participate in the regulation of various biological processes. In this study, we discovered that ankyrin repeat and BTB domain-containing protein 1 (ABTB1) acts as an important regulator of the differentiation of T helper 17 (Th17) cells. ABTB1 deficiency promotes Th17 cell differentiation and exacerbates the symptoms associated with dextran sodium sulfate (DSS)-induced colitis by enhancing Th17 cell-mediated inflammatory responses. Furthermore, the loss of ABTB1 decreases the polyubiquitination of signal transducer and activator of transcription 3 (STAT3) while increasing both the total expression and phosphorylation levels of the STAT3 protein, which are critical for Th17 cell differentiation. On a mechanistic level, this study provides the first evidence that neddylated ABTB1 functions as a novel E3 ubiquitin ligase. Neddylated ABTB1 mediates the K27-, K33-, and K48-linked polyubiquitination of STAT3, thereby promoting its degradation via the ubiquitin-proteasome pathway. Accordingly, ABTB1 inhibits the excessive activation of STAT3 and ultimately suppresses Th17 cell differentiation. Overall, our research demonstrates the critical role of ABTB1 in regulating the differentiation and function of Th17 cells under conditions of autoimmune diseases. Thus, ABTB1 may represent a potential therapeutic target for inflammatory bowel disease (IBD) and other autoimmune disorders.
Background:We analyzed the prevalence and clinical characteristics of children with plastic bronchitis (PB) caused by severe Mycoplasma pneumoniae (SMPP) and explored its risk factors. Methods:This retrospective study included pediatric patients with SMPP who were admitted to the Respiratory Department of Children's Hospital of Soochow University and underwent fiberoptic bronchoscopy (FB) treatment between January 1 and December 31, 2024. The SMPP patients were divided into a PB group and a non-PB group according to whether there was a plastic shape under FB. Epidemiological characteristics, general information, clinical manifestations, laboratory findings, imaging features, and treatment regimens were collected and compared between the two groups. Risk factors for PB were identified using logistic regression analysis, and their predictive value was assessed with receiver operating characteristic (ROC) curves. Results:This study incorporated a total of 510 children diagnosed with SMPP, with 60 and 450 assigned to the PB and non-PB groups, respectively. The epidemic peak of SMPP occurred in summer and autumn; the highest detection rate of PB was recorded in winter (19.30%), with the PB positivity rate peaking in December (32.26%). In the PB group, fever days, runny nose, diminished breath sounds, abnormal liver function, abnormal coagulation function, number of bronchoscopic interventions, neutrophil percentage, C-reactive protein (CRP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), D-dimer, atelectasis, and pleural effusion were all significantly higher compared to the non-PB group (P < 0.05). In the PB group, lymphocyte percentage and platelet count were significantly lower compared to the non-PB group (P < 0.05). Multivariate logistic regression analysis identified LDH, pleural effusion, and length of hospital stay as independent predictors of PB in children. The combination of these three indicators yielded a notably higher predictive value, with an area under the receiver operating characteristics curve (AUC) of 0.911 (95% CI: 0.868∼0.953). Conclusion:LDH, pleural effusion, and length of hospital stay were independent risk factors for PB in SMPP children. For children suspected of PB, pediatricians should pay close attention to the above indicators, strive for early diagnosis and treatment, and improve prognosis.
Objective This study aims to investigate the characteristics of bacterial microbiome in the nasopharynx of children with bronchiolitis and their correlation with recurrent wheezing. Methods The study enrolled children clinically diagnosed with bronchiolitis who were hospitalized in the Respiratory Department of Children's Hospital of Soochow University from October 2021 to March 2022. And we collected their demographic information, clinical data, and laboratory examinations. We collected nasopharyngeal secretions for pathogen examination and nasopharyngeal swabs for detection of nasopharyngeal bacterial microbiome using 16S rDNA sequencing analysis technology. A one-year follow-up was conducted after the children's discharge from the hospital. Based on the occurrence of recurrent wheezing, the children were classified into two groups: recurrent wheezing group and non-recurrent wheezing group. The study aimed to identify differences in pathogens, bacterial microbiome, and other aspects between the two groups. Results There are 13 cases (33.3%) of Human Rhinovirus(HRV) infection in the recurrent wheezing group, which is higher than the 7 cases (13.7%) in the non-recurrent wheezing group( χ 2 = 4.9, P = 0.027). At the genus level, the median abundance of Moraxella in the recurrent wheezing group was 9.2% (0.43, 41%), which was higher than that in the non-recurrent wheezing group at 0.16% (0.09, 0.36%) ( Z =-6.1, P <0.001). Logistic regression analysis showed that eosinophilia count (OR = 49.76, 95% CI 1.2–2018), HRV infection (OR = 13.5, 95% CI 2.6–69), and high abundance of Moraxella catarrhalis in the nasopharynx (OR = 5.2, 95% CI 1.1-25.04) were risk factors for recurrent wheezing in children with bronchiolitis ( p -values were 0.039, 0.002, and 0.041, respectively). Conclusion HRV infection and a high abundance of Moraxella catarrhalis in the nasopharynx are risk factors for subsequent recurrent wheezing in children with bronchiolitis.
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:Cellular senescence has emerged as a key contributor to the pathogenesis of chronic lung diseases. Peroxisome proliferator-activated receptor gamma (PPAR-γ), a nuclear transcription factor, regulates senescence across multiple cell types. However, the role of PPAR-γ in allergic airway inflammation, particularly through regulation of macrophage senescence, remains poorly defined. METHODS:Cellular senescence was evaluated in an allergic asthma mouse model using single-cell RNA sequencing (scRNA-seq). Senescent cells were selectively eliminated with dasatinib and quercetin (D&Q) to assess their contribution to disease pathogenesis. Macrophage-lineage-specific PPAR-γ conditional knockout model (PpargΔCD11c) were generated to define the role of macrophage PPAR-γ in senescence and allergic airway inflammation. PPAR-γ activity was further examined in isolated alveolar macrophages and in vivo using rosiglitazone, including macrophage-targeted delivery via phosphatidylserine-modified liposomes (PSL-ROSI). FINDINGS:scRNA-seq analysis revealed enhanced senescence signatures in mononuclear phagocytes (MNPs), characterised by increased SenMayo scores and elevated Cdkn2a (p16) expression. Clearance of senescent cells significantly reduced airway inflammation and Th2 cytokine levels (IL-4, IL-5). Correlation analysis identified PPAR-γ as a key transcriptional regulator inversely associated with cellular senescence. Macrophage-lineage-specific deletion of PPAR-γ (PpargΔCD11c) exacerbated airway inflammation and increased cellular senescence. In vitro, rosiglitazone reduced allergen-induced senescence and suppressed proinflammatory mediators (IL-6, ICAM-1, CCL4, CCL5, TIMP-1, TNF-α) in alveolar macrophages. In vivo, rosiglitazone and inhaled PSL-ROSI attenuated cockroach allergen-induced airway inflammation, with PSL-ROSI effectively bypassing the airway mucus barrier to deliver rosiglitazone to lung macrophages. Integrated chromatin binding and transcriptomic analyses demonstrated that PPAR-γ promotes macrophage lipid metabolic programs (e.g., CD36, Fabp4). INTERPRETATION:These findings identify macrophage senescence as a pathogenic driver of allergic airway inflammation and establish PPAR-γ as a critical regulator of macrophage senescence and homoeostasis, highlighting its potential as a therapeutic target for asthma. FUNDING:US National Institutes of Health (NIH) (1R01AI153331 and R01AI141642 to Dr. Gao), Anhui Provincial Key projects of Natural Science Foundation for Colleges and Universities 2025AHGXZK31476 (Dr. Wan).
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
Pertussis, caused by Bordetella pertussis, remains a substantial public health threat despite long-standing vaccination programs. Widespread non-pharmaceutical interventions (NPIs) during COVID-19 were accompanied by marked declines in reported pertussis activity in many settings. However, relaxation of containment measures has been followed by resurgence, characterized by atypical outbreak patterns and shifts in case distribution, bacterial genotypes, and affected populations. Emerging evidence suggests that these changes are multifactorial, including altered contact patterns and immunity gap, disruptions and recovery in routine immunization and surveillance, waning or suboptimal vaccine-induced protection, pathogen adaptation, and improved case detection through expanded diagnostic capabilities. Addressing these challenges will require coordinated strategies to restore and optimize immunization delivery, strengthen surveillance and laboratory capacity (including resistance monitoring), and update clinical management guidance in the context of macrolide-resistant B. pertussis. Continued research is needed to define setting-specific drivers and to inform next-generation vaccines and integrated control strategies in the post-pandemic era.
The COVID-19 pandemic substantially altered pediatric respiratory infection patterns. This study assessed the impact of non-pharmaceutical interventions (NPIs) on upper respiratory bacterial epidemiology and microbiota composition in children under 2 years hospitalized with lower respiratory tract infections (LRTIs). Clinical data from 24,159 children admitted between January 2019 and December 2020 were retrospectively analyzed. Following NPI implementation, the overall culture-based bacterial detection rate declined from 61.02% to 18.38%. In an RSV-positive subgroup (pre-COVID-19, n = 95; COVID-19, n = 118), upper respiratory microbiota profiles were characterized using 16S rRNA gene sequencing. Alpha diversity increased significantly, while beta diversity showed distinct community separation between periods (Bray-Curtis distance, PERMANOVA P = 0.01). Taxonomic shifts included increased Proteobacteria and Actinobacteria and reduced Firmicutes, along with decreased Streptococcus and enrichment of Rothia, Dolosigranulum, and Corynebacterium. Overall, NPIs implemented during the COVID-19 pandemic were associated with marked alterations in the upper respiratory bacterial microbiota of RSV-positive young children, highlighting potential implications for future pediatric infection control strategies.
Objective:Upper airway allergic diseases in children refer to chronic non-infectious inflammatory diseases of the upper airway caused by allergic inflammation. These diseases have high prevalences and great harm, furthermore often co-occur. Focusing only on the treatment of individual diseases may lead to ineffective control. To more comprehensively and effectively relieve symptoms and signs, and prevent recurrence or prolongation, pediatric upper airway allergic diseases must be diagnosed and treated jointly as an entity. Although there are currently several guidelines and consensuses on diagnosis and treatment of single pediatric upper airway allergic diseases, there is still a lack of expert consensus on the integrated diagnosis and treatment of multimorbidity. Therefore, the Pediatric Otorhinolaryngology and Head and Neck Surgery Committee of the Chinese Association for the Promotion of Human Health Science and Technology organized multidisciplinary experts to develop this consensus based on clinical experience and evidence-based medicine, aiming to guide the joint diagnosis and treatment of multimorbidity of upper airway allergic diseases in children in clinical practice.