Objective: This study examines the epidemiology of Mycoplasma pneumoniae (M. pneumoniae) infections among children in Suzhou, China, during various pandemic phases. The goal is to discern evolving epidemic trends and to furnish robust evidence for clinical diagnosis and treatment.Methods: From January 1, 2016, to December 31, 2023, 113,625 consecutive patients with respiratory infections from three hospitals in Suzhou, China (Children’s Hospital of Soochow University, Children’s Hospital of Wujiang District, and Affiliated Suzhou Hospital of Nanjing University Medical School), were retrospectively enrolled in a surveillance study. Additionally, in 2023, children hospitalized with M. pneumoniae pneumonia at the Children’s Hospital of Soochow University were tested for genotype (P1 gene typing, SNP genotyping) and macrolide resistance in their bronchoalveolar lavage fluid.Results: From 2016 to 2023, the M. pneumoniae positive detection rate among pediatric respiratory infections fell from a pre-pandemic 21.1% to pandemic lows, then surged to 45.3% post-pandemic. Before the pandemic, peak M. pneumoniae infection rates occurred in summer, followed by autumn. Post-pandemic, the highest peak rates were in autumn. Peak M. pneumoniae detection rates occurred in 2019 and 2023, with a notable increase in children aged 6 and older in 2023. In this study, 200 M. pneumoniae-positive bronchoalveolar lavage fluid (BALF) cases in 2023 were randomly selected and analyzed for P1 genotype and SNP genotype. Among 156 cases, 81.4% were P1 genotype and 18.6% were P2 genotype. The proportion of severe M. pneumoniae pneumonia with the P1 type was significantly higher than that with the P2 type (p < 0.05). Of the 192 samples analyzed, 11 SNP genotypes were identified, with SNP-27 predominating (36.5%), followed by SNP-0 (21.4%), SNP-11 (18.8%), and SNP-34 (17.7%). Of the 192 BALF specimens, 97.3% exhibited macrolide resistance mutations, with A2063G mutations at 96.17%. The mutation rates for the 23S rRNA 2064 and 2,617 were 1.6 and 1.0%, respectively.Conclusion: Post-COVID-19 in Suzhou, China, M. pneumoniae infection patterns shifted significantly, with initial NPIs-induced declines followed by a sharp rise in cases, especially impacting school-age children. This trend underscores the importance of ongoing epidemiological surveillance and the development of strategic public health responses.

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.

Background: Allergic asthma is the most prevalent asthma phenotype and is associated with the disorders of immune cells and glycolysis. Macrophages are the most common type of immune cells in the lungs. Calprotectin (S100A8 and S100A9) are two pro-inflammatory molecules that target the Toll-like receptor 4 (TLR4) and are substantially increased in the serum of patients with severe asthma. This study aimed to determine the effects of S100A8/A9 on macrophage polarization and glycolysis associated with allergic asthma. Methods: To better understand the roles of S100A8 and S100A9 in the pathogenesis of allergic asthma, we used ovalbumin (OVA)-induced MH-S cells, and OVA-sensitized and challenged mouse models (wild-type male BALB/c mice). Enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, flow cytometry, hematoxylin-eosin staining, and western blotting were performed. The glycolysis inhibitor 3-bromopyruvate (3-BP) was used to observe changes in glycolysis in mice. Results: We found knockdown of S100A8 or S100A9 in OVA-induced MH-S cells inhibited inflammatory cytokines, macrophage polarization biomarker expression, and pyroptosis cell proportion, but increased anti-inflammatory cytokine interleukin (IL)-10 mRNA; also, glycolysis was inhibited, as evidenced by decreased lactate and key enzyme expression; especially, knockdown of S100A8 or S100A9 inhibited the activity of TLR4/myeloid differentiation primary response gene 88 (MyD88)/Nuclear factor kappa-B (NF-κB) signaling pathway. Intervention with lipopolysaccharides (LPS) abolished the beneficial effects of S100A8 and S100A9 knockdown. The observation of OVA-sensitized and challenged mice showed that S100A8 or S100A9 knockdown promoted respiratory function, improved lung injury, and inhibited inflammation; knockdown of S100A8 or S100A9 also suppressed macrophage polarization, glycolysis levels, and activation of the TLR4/MyD88/NF-κB signaling pathway in the lung. Conversely, S100A9 overexpression exacerbated lung injury and inflammation, promoting macrophage polarization and glycolysis, which were antagonized by the glycolysis inhibitor 3-BP. Conclusion: S100A8 and S100A9 play critical roles in allergic asthma pathogenesis by promoting macrophage perturbation and glycolysis through the TLR4/MyD88/NF-κB signaling pathway. Inhibition of S100A8 and S100A9 may be a potential therapeutic strategy for allergic asthma.