Abstract:
OBJECTIVE To explore the distribution characteristics of helper T cell subsets in children with bronchopneumonia and analyze the correlation between helper T cell subsets and airway hyperresponsiveness (AHR).
METHODS A total of 183 children with bronchopneumonia admitted to the Affiliated Hospital of Gansu Medical College from Sep. 2019 to Jun. 2024 were selected as the study subjects, and another 63 healthy children during the same period were selected as the control group to compare the distribution of helper T cell subsets between children with bronchopneumonia and healthy children. According to airway responsiveness, children with bronchopneumonia were divided into an AHR group (n=61) and a non-airway hyperresponsiveness (NAHR) group (n=67). Clinical data and the distribution of helper T cell subsets were compared between the two groups. Risk factors for AHR in children with bronchopneumonia were screened, a model was established, and its predictive performance was tested. The interactive effect of risk factors on airway responsiveness was analyzed, and the correlation between helper T cell subsets and airway hyperresponsiveness in children with bronchopneumonia was also analyzed.
RESULTS In the severe group, the levels of helper T lymphocyte (Th) 1, interleukin-2 (IL-2) and interferon-γ (IFN-γ) were (8.72±1.81)%, (6.62±1.22) μg/L and (7.32±1.74) mg/L, respectively, which were lower than those in the mild group and the control group. And the levels of Th2, IL-10, IL-17 and transforming growth factor-β (TGF-β) were (12.06±3.12)%, (23.28±5.68), (46.53±6.69) and (36.24±6.45) ng/L, respectively, which were higher than those in the mild group and the control group (P<0.05). In the mild group, the levels of Th17, IL-10, IL-17 and TGF-β were higher than those in the control group, while the levels of IL-2 and IFN-γ were lower than those in the control group (P<0.05). Disease course (OR=1.536), disease severity (OR=3.267), Th2 level (OR=2.274) and Th17 level (OR=1.772) were identified as risk factors for airway hyperresponsiveness (AHR) in children with bronchopneumonia (P<0.05). The C-index of the model constructed based on these four factors was higher than that of other models. After adjusting confounding factors, Th2 and Th17 levels remained risk factors for AHR in children with bronchopneumonia. As the levels of Th2 and Th17 increased, their associated effect values also increased accordingly (Ptrend<0.001). There was an interaction between the severity of bronchopneumonia and Th2 level in the additive model, and between the severity of bronchopneumonia and Th17 level in both multiplicative and additive models, all demonstrating a synergistic effect.
CONCLUSIONS Th2/Th17 immune imbalance in children with bronchopneumonia is closely related to disease severity and airway hyperresponsiveness, and there are interactions between them. Regulating the Th2/Th17 pathway may represent a new direction for improving airway inflammation in bronchopneumonia.