Journal of Dali University ›› 2023, Vol. 8 ›› Issue (10): 52-58.

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Study on the Mechanism of JAK2-STAT3 Signaling Pathway Mediated by Th1/Th2 Immune Balance Shift in the Occurrence of Infectious Preterm Birth

Du Lingying12Li Zhonglian1Yang Qiongyan1Si Yanting1Guo Ying1*   

  1. 1. The First Affiliated Hospital of Dali UniversityDaliYunnan 671000China2. Maternal and Child Health Hospital of Dali Bai Autonomous PrefectureDaliYunnan 671000China

  • Received:2022-04-25 Revised:2022-06-06 Online:2023-10-15 Published:2023-10-26

Abstract:

ObjectiveTo investigate the Th1/Th2 immune imbalance and the involvement of the JAK2-STAT3 signaling pathway in the mechanism of infectious preterm birth. MethodsA total of 60 preterm patients treated at the First Affiliated Hospital of Dali University were selected as the research objectspreterm group. Based on the results of postpartum fetal membrane tissue pathological examinationthe preterm group was divided into the infectious preterm birth group and non-infectious preterm birth group. 20 puerperae who had full-term deliveries during the same period were selected as the control group. The expression levels of interferon-γ (IFN-γ), interleukin-4 IL-4), interleukin-6 IL-6and tumor necrosis factor-α (TNF-α) in the peripheral blood of the puerperae in the three groups were detected by ELISA kitsand the Th1/Th2 immune regulatory balance index was calculated. The expressions of STAT3 and nuclear factor-κBNF-κBproteins in fetal membrane tissue were detected by immunohistochemistry. ResultsThe expression levels of IFN-γ and TNF-α were significantly elevated in the preterm groupP<0.05), especially in the infectious preterm birth groupindicating that the Th1/Th2 immune balance had a significant shift toward Th1. The expression levels of IL-6STAT3and NF-κB proteins were significantly higher in the infectious preterm birth groupP<0.05), while there was no significant difference between the non-infectious preterm birth group and the control groupP>0.05. ConclusionThe Th1/Th2 immune balance may be involved in the occurrence of infectious preterm birth through TNF-α, NF-κBIL-6 and JAK2-STAT3 signaling pathways.

Key words:

infectious preterm birth, Th1/Th2 immune balance, JAK2-STAT3 signaling pathway

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