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After ending the three-year zero COVID policy in China, the epidemiology of other respiratory pathogens has been affected. This study aimed to characterize of common respiratory pathogen infections in pediatric patients hospitalized for acute respiratory tract infections (ARTIs) in Suzhou before and after ending the zero COVID policy. Nasopharyngeal aspirates (NPAs) were obtained from children with ARTIs (aged ≤ 16 years) at the Children’s Hospital of Soochow University for the detection of respiratory syncytial virus (RSV), influenza A (FluA), FluB, human parainfluenza virus (HPIV), adenovirus (ADV), human rhinovirus (HRV), bocavirus (BoV), human metapneumovirus (HMPV), and mycoplasma pneumoniae (MP). The data were compared between two periods: January 2020 to December 2022 (before ending the zero COVID policy) and January 2023 to May 2024 (after ending the zero COVID policy). Patients were divided into four groups: 0–2, ≥ 3–5, ≥ 6–10, and ≥ 11–16 years. A total of 42,379 patients were enrolled and the top four pathogens identified were MP, HRV, RSV and HPIV with positive rates of 20.2%, 19.5%, 15.1%, and 6.9%, respectively. A total of 28,352 positive cases were detected, with positive rates of 54.0% ( n  = 11,850/21,941) and 80.7% ( n  = 16,502/20,438) before and after ending the zero COVID policy, respectively. Total RSV, HRV, HPIV, and MP positivity increased by 27.8%, 39.0%, 12.3%, and 322.7%, respectively, after ending the zero COVID policy compared to positivity before the policy. After ending the zero COVID policy, the positive rates of RSV, HRV, and HPIV increased most in children aged 0–2 years, with increases by 88.8% (OR: 2.3, 95% CI: 2.2–2.5), 50.0% (OR: 1.6, 95% CI: 1.5–1.7), and 69.6% (OR: 1.8, 95% CI: 1.6-2.0), respectively. The greatest increase in MP positivity was 316.9% in the 3–5 years (OR: 5.5, 95% CI: 4.9–6.1). After ending the zero COVID policy, the RSV-positive rate increased most in summer, while HRV was predominantly circulated in spring and the MP-positive rate peaked in autumn. Ending the zero COVID policy facilitated the transmission of common respiratory pathogens in children. Post-pandemic surveillance and control of respiratory pathogens must be strengthened to reduce health risks.

Objectives: Exosomes are extracellular vesicles released from various inflammatory cells, such as T cells, B cells, dendritic cells (DCs), and mast cells, which have been implicated in the modulation of immune response in asthma. This study aimed to investigate whether exosomes from DCs activated by thymic stromal lymphopoietin (TSLP) play a role in T-helper cell differentiation through the OX40 ligand (OX40L). Methods: Serum samples from patients with asthma were collected to measure the levels of OX40L, T-helper type 1 (Th1) cytokine interferon (IFN)-γ, and T-helper type 2 (Th2) cytokine interleukin (IL)-4 by enzyme-linked immunosorbent assay (ELISA). Exosomes were isolated from TSLP-activated DCs and co-cultured with CD4+ T cells. Western blot and ELISA assays were used to measure the levels of OX40L, IFN-γ, and IL-4 in DCs and CD4+ T cells. Flow cytometry was applied to detect Th1 and Th2 cells. Results: OX40L and IL-4 were increased and IFN-γ was decreased in serum from asthmatic patients compared with healthy controls. TSLP induced DCs to express OX40L in released exosomes, which could promote proliferation of CD4+ T cells, elevate the level of IL-4, and promote Th2 differentiation. Conclusion: Blockade of OX40L in DC-derived exosomes could inhibit exosome-mediated CD4+ T proliferation and Th2 differentiation.

The newly identified Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has resulted in a global health emergency (COVID-19) because of its rapid spread and high mortality. Since the virus epidemic, many pathogenic mechanisms have been revealed, and virus-related vaccines have been successfully developed and applied in clinical practice. However, the pandemic is still developing, and new mutations are still emerging. Virus pathogenicity is closely related to the immune status of the host. As innate immunity is the body’s first defense against viruses, understanding the inhibitory effect of SARS-CoV-2 on innate immunity is of great significance for determining the target of antiviral intervention. This review summarizes the molecular mechanism by which SARS-CoV-2 escapes the host immune system, including suppressing innate immune production and blocking adaptive immune priming. Here, on the one hand, we devoted ourselves to summarizing the combined action of innate immune cells, cytokines, and chemokines to fine-tune the outcome of SARS-CoV-2 infection and the related immunopathogenesis. On the other hand, we focused on the effects of the SARS-CoV-2 on innate immunity, including enhancing viral adhesion, increasing the rate of virus invasion, inhibiting the transcription and translation of immune-related mRNA, increasing cellular mRNA degradation, and inhibiting protein transmembrane transport. This review on the underlying mechanism should provide theoretical support for developing future molecular targeted drugs against SARS-CoV-2. Nevertheless, SARS-CoV-2 is a completely new virus, and people’s understanding of it is in the process of rapid growth, and various new studies are also being carried out. Although we strive to make our review as inclusive as possible, there may still be incompleteness.

Background Co-infections are common in childhood community acquired pneumonia (CAP). However, their etiological pattern and clinical impact remains inconclusive. Methods Eight hundred forty-six consecutive children with CAP were evaluated prospectively for the presence of viral and bacterial pathogens. Nasopharyngeal aspirates were examined by direct immunofluorescence assay or polymerase chain reaction (PCR) for viruses. PCR of nasopharyngeal aspirates and enzyme-linked immunosorbent assays were performed to detect M. pneumoniae. Bacteria was detected in blood, bronchoalveolar lavage specimen, or pleural fluid by culture. Results Causative pathogen was identified in 70.1% (593 of 846) of the patients. The most commonly detected pathogens were respiratory syncytial virus (RSV) (22.9%), human rhinovirus (HRV) (22.1%), M. pneumoniae (15.8%). Coinfection was identified in 34.6% (293 of 846) of the patients. The majority of these (209 [71.3%] of 293) were mixed viral-bacterial infections. Age < 6 months (odds ratio: 2.1; 95% confidence interval: 1.2–3.3) and admission of PICU (odds ratio: 12.5; 95% confidence interval: 1.6–97.4) were associated with mix infection. Patients with mix infection had a higher rate of PICU admission. Conclusions The high mix infection burden in childhood CAP underscores a need for the enhancement of sensitive, inexpensive, and rapid diagnostics to accurately identify pneumonia pathogens.

Tea oil tree (Camellia oleifera), a woody oil crop native to Southern China, relies on insect pollination for fruit and seed production. However, its nectar is toxic to honey bees (Apis spp.) due to their inability to digest the oligosaccharide present in the nectar. This toxicity raises concerns about the trade-off between the benefits of pollination and the risks posed by exposures to toxic nectar. We aimed to investigate whether tea oil tree yield is enhanced by honey bee pollination, while also examining the impact of nectar toxicity and exploring potential mitigation methods. We evaluated the fruit set, seed yield, and oil quality of the crop with or without eastern honey bee (A. cerana) pollination during 2019–2022. We also characterized nectar oligosaccharide compositions collected from both flowers and bee hives. We administered α-galactosidase (an enzyme to promote oligosaccharide digestion) onto bee larvae fed with crop nectar. We found that A. cerana could significantly enhance fruit set and seed yield. The administration of α-galactosidase could enhance larval survivorship challenged by nectar toxicity. The effectiveness of honey bee pollination can vary between years, with warmer temperatures significantly enhancing honey bee pollination benefits. The results suggest that a decision to use honey bees for pollinating tea oil trees should involve consideration of the impact of local weather conditions, as low temperatures may compromise pollination benefits while increasing risks posed by toxic nectar. The administration of digestive enzymes to honey bees shows potential for mitigating natural toxins in tea oil tree nectar.

Objective To determine the risk factors for delayed radiographic resolution in children with refractory Mycoplasma pneumoniae pneumonia (RMPP) and explore the most suitable time for interventional bronchoscopy. Methods This retrospective study involved 142 children with RMPP who were admitted to our hospital from 1 January 2015 to 31 December 2017. They were divided into a common resolution group and a delayed resolution group based on their chest radiograph series. Results Among the 142 patients, 67 showed common resolution on chest radiographs and 75 showed delayed resolution. Independent risk factors for delayed resolution were a clinical course of ≥11.5 days before the performance of interventional bronchoscopy, mucus plug formation, corticosteroid resistance, and atelectasis. When bronchoscopy was performed before the disease had been present for <11.5 days, the length of hospitalization, total fever duration, and duration of time until disappearance of coughing were shorter than those in children who underwent bronchoscopy after the disease had been present for ≥11.5 days. Conclusions Corticosteroid resistance, the time to interventional bronchoscopy, atelectasis, and mucus plug formation were associated with delayed resolution on chest radiographs. Performance of interventional bronchoscopy before the clinical course has reached 11.5 days may help alleviate clinical symptoms and improve radiographic resolution.

Objective We aimed to develop a nomogram to predict the risk of severe influenza in previously healthy children. Methods In this retrospective cohort study, we reviewed the clinical data of 1135 previously healthy children infected with influenza who were hospitalized in the Children's Hospital of Soochow University between 1 January 2017 and 30 June 2021. Children were randomly assigned in a 7:3 ratio to a training or validation cohort. In the training cohort, univariate and multivariate logistic regression analyses were used to identify risk factors, and a nomogram was established. The validation cohort was used to evaluate the predictive ability of the model. Result Wheezing rales, neutrophils, procalcitonin > 0.25 ng/mL, Mycoplasma pneumoniae infection, fever, and albumin were selected as predictors. The areas under the curve were 0.725 (95% CI: 0.686–0.765) and 0.721 (95% CI: 0.659–0.784) for the training and validation cohorts, respectively. The calibration curve showed that the nomogram was well calibrated. Conclusion The nomogram may predict the risk of severe influenza in previously healthy children.

Background Bronchiolitis is a clinical syndrome commonly encountered in practice, particularly among infants and young children. To investigate the prevalence of pathogens in hospitalized children with bronchiolitis and study the clinical characteristics of bronchiolitis with or without coinfections. Methods We investigated the respiratory specimens and clinical data of 1012 children with bronchiolitis who were treated at the Children’s Hospital of Soochow University between November 2011 and December 2018. The nasopharyngeal aspirates were examined to detect viruses by direct immunofluorescence assay or polymerase chain reaction (PCR). Mycoplasma pneumoniae (MP) was tested by PCR and enzyme-linked immunosorbent assay. Results Of the 1134 children less than 2 years with bronchiolitis, 122 were excluded by exclusion criteria. Causative pathogen was detected in 83.2% (842 of 1012). The majority of these (614 [72.9%] of 842) were single virus infection. The most common pathogens detected were respiratory syncytial virus (RSV) (44.4%), MP (15.6%), and human rhinovirus (HRV) (14.4%). Coinfection was identified in 13.5% (137 of 1012) of the patients. Coinfection included mixed virus infection and virus infection with MP infection. Children with single virus infection had a higher rate of oxygen therapy compared with single MP infection. Conclusions The most common pathogen detected in children with bronchiolitis is RSV, followed by MP and HRV. Coinfection leads to a longer period of illness, increased severity of the symptoms and increased risk of hypoxemia.

China had its first wave of COVID-19 in 2020 and second wave of COVID-19 Omicron in 2022. The number of RSV cases decreased sharply in 2020 and 2022. Investigation of the resurge of RSV infections after the first wave of COVID-19 will guide us to take preventive actions before the resurge of RSV infections after the second wave of COVID-19 Omicron. We analysed epidemiological and clinical data of 59934 patients with lower respiratory tract infections (LRTI) from a prospective long-term cohort surveillance programme in Suzhou, China, collected from February 2016 to January 2022. The annual incidence of RSV infection in children aged<16 years in 2020 and 2021 was compared with the pre-pandemic years 2016 to 2019. We also compared the clinical characteristics, and RSV-related ICU admissions between pre-pandemic years and 2021. Among children with LRTI, the positive rate of RSV increased by 70.7% in 2021 compared to the average level in the pre-pandemic years. The RSV resurge in 2021 was most prominently in children aged 2-4 years (a significant rise compared with the expected value 149.1%; 95%CI, 67.7% to 378%, P<.01). The percentage of RSV-related ICU admissions decreased in 2021 (3.2% vs 6.7%, P<0.01). The death rate of RSV infections in 2021 was 0.2%, while that in pre-pandemic years was only 0.02%. RSV-associated death in immunocompetent children (complicated by necrotizing encephalitis) was firstly occurred in 2021. Our findings raise concerns for RSV control in Southeast China after the COVID-19 pandemic especially for children aged 2-4 years. Although ICU admissions were significantly reduced in this resurgence, we could not ignore the increase of RSV-associated death.

Within the past 3-5 years, has become a major pathogen of community-acquired pneumonia in children. The pathogenic mechanisms involved in infection have not been fully elucidated. Previous protein microarray studies have shown a differential expression of CXCL9 after infection. Here, we conducted a hospital-based study to explore the clinical significance of the type 1 immune response inflammatory factors interferon (IFN)-γ and CXCL9 in patients with pneumonia (MPP). Then, through experiments, we explored whether CARDS toxin stimulated F-DCs (dendritic cells incubated with Flt3L) to promote Th-cell differentiation; we also investigated the IFN-γ-induced CXCL9 secretion pathway in macrophages and the role of CXCL9 in promoting Th1 cell migration. The CXCL9 expression level was upregulated among patients with a higher fever peak, fever duration of greater than 7 days, an imaging manifestation of lobar or segmental, or combined pleural effusion ( <0.05). The peripheral blood levels of IFN-γ and CXCL9, which were higher in patients than in the healthy control group, were positively correlated with each other ( =0.502, <0.05). In patients, the CXCL9 expression level was significantly higher in the bronchoalveolar lavage fluid (BALF) than in the peripheral blood, and the BALF CXCL9 expression level was higher than that in the healthy control group (all <0.05). Our flow cytometry analysis revealed that M1-phenotype macrophages (CD16 CD64 CD163 ) were predominant in the BALF from children with MPP. In experiments, F-DCs stimulated with CARDS toxin promoted the differentiation of CD4 IFN-γ Th (Th1) cells ( <0.05). Moreover, IFN-γ induced high levels of CXCL9 expression in M1-type macrophages in a dose-dependent and time-dependent manner. Additionally, macrophages transfection with STAT1-siRNA-1 downregulated the expression of CXCL9 ( <0.05), and CXCL9 promoted Th1 cell migration ( <0.05). Our findings suggest that CARDS toxin induces a type 1 immune response positive feedback loop during infection; this putative mechanism may be useful in future investigations of immune intervention approaches for pneumonia.