Objective To detect the levels of tumor necrosis factor (TNF)-a,interleukin (IL)-1β,IL-2,1L-6,IL-8,1L-10,IL-12 and interferon (IFN)-α in the serum and cerebrospinal fluid of the patients with epidemic encephalitis B,and to investigate the roles in pathogenesis of epidemic encephalitis B.Methods Approximately of 2 mL serum and 2 mL cerebrospinal fluid from 24 patients with epidemic encephalitis B during acute phase were collected,and 2 mL serum from 20 healthy controls were collected.The levels of eytokines in serum and cerebrospinal fluid were detected by enzyme linked immunosorbent assay (ELISA).Means of multi-sample were compared by analysis of variance and means of two-sample were compared by t test.Results The levels of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-α in eerebrospinal fluid were (24.5±6.6),(7.8±2.4),(16.0±5.7),(17.6±4.8),(130.2±33.6) and (45.2±10.8) ng/L,respectively,and in serum were (25.3±11.2),(7.1±3.2),(14.5±6.2),(16.0±6.5),(82.0±27.8) and (42.5±16.2) ng/L,respectively.The levels of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-α in serum and cerebrospinal fluid from patients with epidemic encephalitis B were all higher than those in serum of healthy controls [(12.7±7.9),(2.6±1.0),(6.2±2.2),(9.6±3.3),(71.4±12.8) and (30.0±14.0) ng/L;F value was 14.10,29.46,23.38,14.78,32.59,7.52;all P＜0.01];while the levels of IL-2 and IL-12 were not increased significantly.The levels of IL-1β,IL-6,IL-8,IL-10,IL-12 and IFN-α in cerebrospinal fluid were higher than those in serum,while the levels of TNF-± and IL-2 in cerebrospinal fluid were lower than those in serum.The levels of IL-6 and IL-8 in cerebrospinal fluid from patients with severe type of epidemic encephalitis B were (18.8±5.4) ng/L and (20.7±2.7) ng/L,and were higher than those with common type [(12.1±3.0) and (13.3±3.3) ng/L;t=3.50,t=5.96;P＜0.05],while the levels of IL-2 in serum and in cerebrospinal fluid from patients with severe type were lower than those with common type. Conclusions Oversecretions of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-a are involved in the inflammatory damage of epidemic encephalitis B,while under-secretions of IL 2 and ILl2 may be involved in cellular immune responses.

Objective To explore the role and mechanism of the exosomes derived from bronchoalveolar lavage fluid(BALF)of patients with chronic obstructive pulmonary disease(COPD-Exo)in regulating osteoblast differentiation.Methods A total of 6 COPD patients and 6 non-COPD patients admitted in our hospital in June 2023 were recruited,and their BALF samples were collected during the process.COPD-Exo and exosomes from the non-COPD patients(Ctrl-Exo)were extracted and identified by electron microscopy and Western blotting.Alizarin red staining and qRT-PCR were used to detect the differences in osteoblast differentiation after COPD-Exo and Ctrl-Exo intervention.Bioinformatics analysis was performed on the microRNA(miRNA)expression profiles of COPD-Exo and Ctrl-Exo in the GEO database(GSE218571)to obtain differentially expressed miRNAs.Antagomir was used to block mircoRNA function,and the miRNAs with osteogenic differentiation regulatory function were identified.Targetscan software was used to predict the downstream target genes of the miRNAs,and then these miRNAs were verified.Results Exo could be extracted from BALF of both COPD and non-COPD patients.Alizarin red staining and qRT-PCR results showed that COPD-Exo inhibited the osteogenic differentiation of human hFOB 1.19 osteoblasts(P＜0.05).Bioinformatics analysis indicated that the expression level of miR-223-3p was significantly up-regulated in COPD-Exo.Blocking miR-223-3p with Antagomir could alleviate the osteogenic differentiation of human hFOB 1.19 osteoblasts inhibited by COPD-Exo(P＜0.05).Targetscan prediction revealed that miR-223-3p may target and inhibit the expression of osteogenic differentiation-related factor FOXO3(P＜0.05).Conclusion COPD-Exo can inhibit the osteogenic differentiation of human hFOB 1.19 osteoblasts through miR-223-3p,which may be related to the inhibition of FOXO3 expression by miR-223-3p.