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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.

In a phase 3 trial involving infants in China, ziresovir, an orally administered RSV F protein inhibitor, led to an improvement in the Wang bronchiolitis score at day 3 and a decline in the RSV viral load by day 5.

Long non-coding RNAs (lncRNAs) play a crucial role in macrophage development but little is known about their role in asthma. Here, we investigated the role of lncRNA lncTRPM2-AS in asthma and found that lncTRPM2-AS participates in the promotion of macrophage inflammation. Downregulation of lncTRPM2-AS promoted apoptosis and inhibited proliferation and production of cytokines including IL-1β, IL-4, IL-6, IL-10, TNF-α, and TGF-β. RNA-immunoprecipitation and mass spectrometry indicated that the protein TRPM2 interacted with both lncTRPM2-AS and the E3 ubiquitin ligase TRIM21. LncTRPM2-AS silencing enhanced the interaction between TRIM21 and TRPM2, resulting in elevated levels of ubiquitin-related degradation of TRPM2. Mutation analysis indicated that TRPM2 K1218 is a key site for TRIM21-dependent ubiquitination. Downregulation of lncTRPM2-AS significantly decreased intracellular calcium levels by restraining TRPM2 protein expression, which in turn decreased ROS levels and increased autophagy to promote macrophage apoptosis and reduce cytokine production, together inhibiting macrophage inflammation. Taken together, our findings demonstrate that lncTRPM2-AS blocks the ubiquitination of TRPM2 via TRIM21 and inhibits autophagy-induced apoptosis which may contribute to macrophage inflammation in asthma.

Background Infants with bronchiolitis have an increased risk of developing recurrent wheezing and asthma. However, the risk factors for the development of recurrent wheezing after bronchiolitis remains controversial. Our study was to investigate risk factors of post-bronchiolitis recurrent wheezing. Methods Infants with bronchiolitis were enrolled from November 2016 through March 2017. Nasopharyngeal aspirates were obtained for detection of respiratory viruses which were analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) and direct immunofluorescent assay. Serum cytokines including TSLP, IL2, IL13, TIMP-1, MMP-9, IL33, IL5, IL4, IL25, TNF- α and MIP-1α were measured by flow cytometry. Patients were followed up every 3 months for a duration of 2 years by telephone or at outpatient appointments. Results We enrolled 89 infants, of which 81 patients were successfully followed up. In total, 22.2% of patients experienced recurrent wheezing episodes. The proportion of patients with history of eczema, systemic glucocorticoid use and patients with moderate-to-severe disease were significantly higher in the recurrent wheezing group than the non-recurrent wheezing group (83.3% vs 52.4%; 66.7% vs 36.5%; 61.1% vs 33.3%, respectively, all P  < 0.05); There were no significant differences between patients with and without recurrent wheezing episodes in the levels of TSLP, IL2, IL13, TIMP-1, MMP-9, IL33, IL5, IL4, IL25, TNF- α and MIP-1α ( P  > 0.05). Logistic regression analysis showed that history of eczema was an independent risk factor for post-bronchiolitis recurrent wheezing (odds ratio [OR] = 5.622; 95% confidence interval [CI], 1.3–24.9; P  = 0.023). Conclusion The incidence of recurrent wheezing among infants after contracting bronchiolitis was 22.2% during a 2-year follow-up. History of eczema was the only independent risk factor identified and no correlation was found between the specific virus and disease severity in children with post-bronchiolitis recurrent wheezing.

To investigate the impact of viral and bacterial co-infection in hospitalised children with Mycoplasma pneumoniae pneumonia (RMPP). Retrospective analysis of 396 children with RMPP in our hospital admitted between 1 January 2011 and 31 December 2016 was performed. Nasal aspirate samples were collected for pathogen detection and clinical data were collected. We analysed clinical characteristics, lung imaging characteristics and pathogenic species among these children. Of the 396 RMPP cases, 107 (27.02%) had co-infection with other pathogen, with Streptococcus pneumoniae, Haemophilus influenzae and Staphylococcus aureus being the most common bacteria of infection and human bocavirus (HBoV), human rhinovirus, respiratory syncytial virus being the most common viruses of infection. Children with co-infection were younger than that with single infection (P = 0.010). Children with both virus and bacteria co-infection had been the youngest (P = 0.040). Children with co-infection had a longer fever process, higher leukocyte count, higher C-reactive protein compared with single infection (P < 0.05). Children with co-infection had a higher percentage of pnemothorax and diffuse large area of inflammation in chest X-ray manifestation compared with children with single infection (P < 0.05). S. pneumonia and HBoV was the leading cause of co-infection in RMPP. Co-infections led to more disease severity in children with RMPP compared with single infections.

Background Early distinction between refractory M. pneumoniae pneumonia (RMPP) and non-RMPP (NRMPP) is still difficult. The community-acquired respiratory distress syndrome (CARDS) toxin can induce inflammatory and histopathological phenotypes associated with M. pneumoniae infection. This study aimed to investigate the clinical significance of CARDS toxin and pro-inflammatory cytokines in children with RMPP and to explore whether CARDS toxin can induce TNF-α expression. Methods Levels of CARDS toxin and cytokines in BALF from control and children with MPP were determined by real-time PCR and ELISA, respectively. A receiver-operating characteristic (ROC) analysis was performed to assess the diagnostic values of CARDS toxin, TNF-α, and IL-6 in RMPP. The recombinant CARDS toxin was constructed and prepared at different concentrations for stimulation of RAW264.7 cells. After co-culture with CARDS toxin, cytokines were detected by ELISA and the mRNA levels were measured by real-time PCR. Effects of CARDS toxin and TNF-α on inflammatory cell infiltration and mucus secretion in mouse lungs were also evaluated. Results Levels of CARDS toxin, TNF-α and IL-6 in bronchoalveolar lavage fluid (BALF) were significantly higher in RMPP cases compared with NRMPP cases. Furthermore, TNF-α had better diagnostic ability for differentiation of RMPP with AUC of 0.824 and Youden index of 0.692 compared with CARDS toxin and IL-6. Moreover, CARDS toxin was positively correlated with TNF-α level in MPP cases. In vitro assay revealed that CARDS toxin induced RAW264.7 macrophages to secrete TNF-α. Further in vivo assay showed that TNF-α deletion partially abrogated the CARDS toxin-mediated induction of inflammatory cell infiltration and mucus secretion in mouse lungs. Conclusions The high co-expression of TNF-α and CARDS toxin in BALF is a good diagnostic biomarker for differentiating children with RMPP and NRMPP.

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.

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.

Neutrophil infiltration is the characteristic pathological feature of M. pneumoniae pneumonia (MPP). This study aimed to explore the associations among neutrophil activity, clinical presentation, and role of the M. pneumoniae/interleukin-8 (IL-8)/neutrophil axis in the pathogenesis of MPP. A total of 42 patients with MPP were prospectively enrolled in the study. Neutrophil activity, including matrix metalloproteinase-9 (MMP-9), myeloperoxidase (MPO), and neutrophil elastase (NE), were measured. Clinical information was collected for all patients and control group. In vitro, IL-8 production was measured at different time points after M. pneumoniae infection of bronchial epithelial cells, and neutrophil activity was analyzed after IL-8 stimulation. The percentage of neutrophil in the bronchoalveolar lavage fluid was higher in the group of patients with high levels of M. pneumoniae DNA than in those with low levels of M. pneumoniae DNA (P < 0.05). IL-8, MMP-9, and NE in patients with MPP significantly increased compared with controls and decreased after treatment (P < 0.05). MPO and MMP-9 were associated with duration of fever (r = 0.332, P < 0.05) and length of stay (r = 0.342, P < 0.05), respectively. In vitro, M. pneumoniae induced IL-8 production by bronchial epithelial cells in a time dependent manner. MPO, MMP-9 and NE production by neutrophils significantly increased compared with medium controls after IL-8 stimulation. In summary, the M. pneumoniae/IL-8/neutrophil axis likely plays a vital role in the pathogenesis of MPP.