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Objective To investigate the changes and significance of Toll-like receptor 7 （TLR7）， TLR9 and type I interferon （IFN-Ⅰ） in children with severe mycoplasma pneumoniae pneumonia （SMPP）. Methods 80 children with mycoplasma pneumoniae pneumonia （MPP） were divided into the non-severe MPP （MPP group） and SMPP groups （SMPP group）. 26 healthy children who underwent outpatient physical examination were chosen as the control group. Serum samples in each group were collected. In the SMPP group， bronchoalveolar lavage fluid （BALF） on the affected and contralateral sides of 26 children with unilateral lung consolidation， atelectasis， lung abscess or lung tissue necrosis on imaging examination were collected. The levels of TLR7， TLR9， myeloid differentiation factor 88 （MyD88）， interferon-α （IFN-α） and IFN-β in the serum and BALF samples were determined by enzyme-linked immunosorbent assay （ELISA）. Results The serum levels of TLR7， TLR9， MyD88， IFN-α and IFN-β in the SMPP and MPP groups were significantly higher than those in the control group， and the levels of all cytokines in the SMPP group were significantly higher compared with those in the MPP group （all P < 0.05）. The levels of TLR7， TLR9， MyD88， IFN-α and IFN-β in the BALF on the affected side were significantly higher than those on the contralateral side （all P < 0.01）. The area under the receiver operating characteristic curve （AUC） of serum TLR7 and MyD88 levels for predicting SMPP was 0.709 and 0.723. Conclusions Over-induced and generated TLR7， TLR9， IFN-α and IFN-β may be pathogenic factors for the incidence of SMPP and severe local lung tissue injury in children with SMPP. TLR7 and MyD88 can be used as predictors of SMPP to guide clinical treatment.

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Objectives: To explore the role of the cGAS-STING signaling pathway in the therapeutic mechanism of Liangxue Jiedu Huayu Formula (LXJDHYF) for acute-on-chronic liver failure (ACLF) in mice., Methods: Thirty C57BL/6 mice were randomly divided into blank control group, model group, low- and high-dose LXJDHYF groups, and H151 (a specific cGAS-STING pathway inhibitor) group ( n= 6). In all but the control group, the mice were treated with CCl 4 to induce liver cirrhosis followed by intraperitoneal injections of lipopolysaccharide and D-amino galactose to establish mouse models of ACLF. After the treatments, the mouse livers were collected for HE and TUNEL staining, and serum levels of ALT, AST and TBil were determined. In bone marrow-derived macrophages (BMDMs) and liver tissues of ACLF mice, the expressions of cGAS-STING signaling pathway-related mRNAs including IFN‑β, ISG15, IL-6 and TNF-α were determined with RT-qPCR, and the phosphorylation levels of IRF3 and STING proteins were investigated using Western blotting., Results: Compared with the mice in the model group, the LXJDHYF-treated mice exhibited milder hepatocyte necrosis and inflammatory cell infiltration in the liver with significantly reduced hepatocyte apoptosis. LXJDHYF treatment also significantly lowered serum levels of ALT, AST, TBil, IL-6 and TNF-α in ACLF mice and effectively suppressed the expressions of cGAS-STING signaling pathway-related mRNA in both the BMDMs and the liver tissues and the phosphorylation of IRF3 and STING proteins in the BMDMs., Conclusions: LXJDHYF can significantly improve liver function and attenuate inflammation in ACLF mice possibly by inhibiting excessive activation of the cGAS-STING signaling pathway.