Role of the Notch ligand DLL4 in the immune response of children with Mycoplasma pneumoniae pneumonia
DOI:
https://doi.org/10.1590/S1678-9946202567065Keywords:
Mycoplasma pneumoniae, Pneumonia, Notch, DLL4, Cytokines, Lymphocyte subsetsAbstract
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.
Downloads
Downloads
Published
Issue
Section
License
Copyright (c) 2025 Heting Dong, Zhiao Du, Yaru Liao, Jiying Sun, Huiming Sun, Peng Mo, Ge Dai, Li Huang, Feng Huang, Chuangli Hao, Zhengrong Chen, Yongdong Yan

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.