Objectives To elucidate the potential role of cytokines in the pathogenesis of coro- nary heart disease (CHD). Methods TNF-α and IFN-γ activity , IL-8 levels of plasma and supematants were measured in 62 patients wi...Objectives To elucidate the potential role of cytokines in the pathogenesis of coro- nary heart disease (CHD). Methods TNF-α and IFN-γ activity , IL-8 levels of plasma and supematants were measured in 62 patients with CHD and 30 health controls by methods of direct cytotoxicity assay, cyto- pathic effect inhibition test and ELISA respectively. Results Both TNF-α activity and IL-8 levels of plas- ma in CHD patients were higher and IFN-γ activity of supematants in CHD patients were lower than those of healthy controls(P < 0.001),There have significant differences between healthy controls and the subgroups of CHD ( P < 0. 01 ) . IL-8 levels of plasma increased with the advancing of the disease and there have obvious differences among subgroups of the illness(P <0. 05). TNF-α activity of plasma in stable angina pectoris ( SAP ) subgroup was lower than those of unstable an- gina pectoris ( UAP ) and acute myocardial infarction ( AMI) subgroups, the differences between SAP and UAP or AMI were significant ( P < 0. 05 ) , But there have no significant differences between UAP and AMI (P> 0. 05). However, IFN-γ activity of supematants showed no difference among any subgroups. Conclu- sions there have close relations between TNF-α, IFN-γ,IL-8 and CHD.展开更多
AIM: To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS: The oxygen-induced retinopathy(OIR) mouse mod...AIM: To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS: The oxygen-induced retinopathy(OIR) mouse model and the human Moorfield/Institute of Ophthalmology-Müller 1(MIO-M1) cell line were used in the study. Immunofluorescence staining was used to determine the distribution and expression of periostin and a Müller glial cell marker glutamine synthetase(GS). Cytokines TNF-α and IFN-γ were added to stimulate the MIO-M1 cells. ShRNA was used to knockdown periostin expression in MIO-M1 cells. Quantitative real-time reverse transcription polymerase chain reaction(qRT-PCR) was conducted to assess the mRNA expression of periostin. RESULTS: Immunofluorescence staining showed that periostin was expressed by MIO-M1 Müller glia. GS-positive Müller glia and periostin increased in OIR retinas, and were partially overlaid. The stimulation of TNF-α and IFN-γ reduced the mRNA expression of periostin significantly and dose-dependently in MIO-M1 cells. Knockdown of periostin reduced mRNA expression of vascular endothelial growth factor A(VEGFA) in MIO-M1 cells, while VEGFA expression was not changed in periostin knock-out OIR retinas. CONCLUSION: Müller glia could be one of the main sources of periostin in the retina, and might contribute to the pathogenesis of retinal neovascularization. Proinflammatory cytokines TNF-α and IFN-γ attenuate the periostin expression in retinal Müller glia, which provides a potential and novel method in treating retinal neovascular diseases.展开更多
AIM: To approach the relationship between alveolar echinococcosis (AE) pathology and level of sIL-2R,TNF-α and IFN-γ in sera and the significance of cytokines in development of AE.METHODS: After 23 patients with AE ...AIM: To approach the relationship between alveolar echinococcosis (AE) pathology and level of sIL-2R,TNF-α and IFN-γ in sera and the significance of cytokines in development of AE.METHODS: After 23 patients with AE were confirmed by ELISA and ultrasound, their sera were collected and the concentrations of sIL-2R,TNF-α and IFN-γ were detected by double antibody sandwich. Twelve healthy adults served as controls. According to the status of livers of AE patients by ultrasound scanning, they were divided into 4 groups: P2,P3, P4 groups and C group (control). Average of concentrations of sIL-2R, TNF-α and IFN-yin homologous group was statistically analyzed by both ANOV and Newman-Keuls, respectively.RESULTS: The mean of sIL-2R in P2 group was 97±29, P3:226±80, P4:194±23 and control group (111±30)×10^3 u/L(P<0.01). The mean of TNF-α in P2 group was 1.12±0.20, P3:3.67±1.96, P4:1.30±0.25 and control group 0.40±0.19 μg/L(P<0.01). The mean of IFN-γ in P2 group was 360±20, P3:486±15, P4:259±19 and control group: 16±2 ng/L (P<0.01).Judged by ANOV and Newman-Keuls, the mean concentrations of sIL-2R, TNF-α and IFN-γ had a significant difference among groups. Except for P2group, the mean sIL-2R between other groups of AE patients had a significant difference (P<0.05). The mean of TNF-α concentration in P3 group was the highest (P<0.01). The mean of IFN-γ concentration in all patients was higher than that in control group (P<0.01),but there was no difference between AE groups (P>0.05).CONCLUSION: Low sIL-2R level indicates an early stage of AE or stable status, per contra, a progression stage. Higher level of TNF-α might be related to the lesion of liver. The role of single IFN-γ is limited in immunological defense against AE and it can not fully block pathological progression.展开更多
文摘Objectives To elucidate the potential role of cytokines in the pathogenesis of coro- nary heart disease (CHD). Methods TNF-α and IFN-γ activity , IL-8 levels of plasma and supematants were measured in 62 patients with CHD and 30 health controls by methods of direct cytotoxicity assay, cyto- pathic effect inhibition test and ELISA respectively. Results Both TNF-α activity and IL-8 levels of plas- ma in CHD patients were higher and IFN-γ activity of supematants in CHD patients were lower than those of healthy controls(P < 0.001),There have significant differences between healthy controls and the subgroups of CHD ( P < 0. 01 ) . IL-8 levels of plasma increased with the advancing of the disease and there have obvious differences among subgroups of the illness(P <0. 05). TNF-α activity of plasma in stable angina pectoris ( SAP ) subgroup was lower than those of unstable an- gina pectoris ( UAP ) and acute myocardial infarction ( AMI) subgroups, the differences between SAP and UAP or AMI were significant ( P < 0. 05 ) , But there have no significant differences between UAP and AMI (P> 0. 05). However, IFN-γ activity of supematants showed no difference among any subgroups. Conclu- sions there have close relations between TNF-α, IFN-γ,IL-8 and CHD.
基金Supported by National Natural Science Foundation of China(No.81800855 No.81800856+4 种基金 No.81700837)Natural Science Foundation of Hunan Province(No.2018JJ3765)Department of Science and Technology,Hunan(No.2015TP2007)Japan Society for the Promotion of Science KAKENHI Grants(No.26293374 No.16K15734)
文摘AIM: To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS: The oxygen-induced retinopathy(OIR) mouse model and the human Moorfield/Institute of Ophthalmology-Müller 1(MIO-M1) cell line were used in the study. Immunofluorescence staining was used to determine the distribution and expression of periostin and a Müller glial cell marker glutamine synthetase(GS). Cytokines TNF-α and IFN-γ were added to stimulate the MIO-M1 cells. ShRNA was used to knockdown periostin expression in MIO-M1 cells. Quantitative real-time reverse transcription polymerase chain reaction(qRT-PCR) was conducted to assess the mRNA expression of periostin. RESULTS: Immunofluorescence staining showed that periostin was expressed by MIO-M1 Müller glia. GS-positive Müller glia and periostin increased in OIR retinas, and were partially overlaid. The stimulation of TNF-α and IFN-γ reduced the mRNA expression of periostin significantly and dose-dependently in MIO-M1 cells. Knockdown of periostin reduced mRNA expression of vascular endothelial growth factor A(VEGFA) in MIO-M1 cells, while VEGFA expression was not changed in periostin knock-out OIR retinas. CONCLUSION: Müller glia could be one of the main sources of periostin in the retina, and might contribute to the pathogenesis of retinal neovascularization. Proinflammatory cytokines TNF-α and IFN-γ attenuate the periostin expression in retinal Müller glia, which provides a potential and novel method in treating retinal neovascular diseases.
基金Supported by the STD3 Programme of the EC,No.TS3-CT94-0270
文摘AIM: To approach the relationship between alveolar echinococcosis (AE) pathology and level of sIL-2R,TNF-α and IFN-γ in sera and the significance of cytokines in development of AE.METHODS: After 23 patients with AE were confirmed by ELISA and ultrasound, their sera were collected and the concentrations of sIL-2R,TNF-α and IFN-γ were detected by double antibody sandwich. Twelve healthy adults served as controls. According to the status of livers of AE patients by ultrasound scanning, they were divided into 4 groups: P2,P3, P4 groups and C group (control). Average of concentrations of sIL-2R, TNF-α and IFN-yin homologous group was statistically analyzed by both ANOV and Newman-Keuls, respectively.RESULTS: The mean of sIL-2R in P2 group was 97±29, P3:226±80, P4:194±23 and control group (111±30)×10^3 u/L(P<0.01). The mean of TNF-α in P2 group was 1.12±0.20, P3:3.67±1.96, P4:1.30±0.25 and control group 0.40±0.19 μg/L(P<0.01). The mean of IFN-γ in P2 group was 360±20, P3:486±15, P4:259±19 and control group: 16±2 ng/L (P<0.01).Judged by ANOV and Newman-Keuls, the mean concentrations of sIL-2R, TNF-α and IFN-γ had a significant difference among groups. Except for P2group, the mean sIL-2R between other groups of AE patients had a significant difference (P<0.05). The mean of TNF-α concentration in P3 group was the highest (P<0.01). The mean of IFN-γ concentration in all patients was higher than that in control group (P<0.01),but there was no difference between AE groups (P>0.05).CONCLUSION: Low sIL-2R level indicates an early stage of AE or stable status, per contra, a progression stage. Higher level of TNF-α might be related to the lesion of liver. The role of single IFN-γ is limited in immunological defense against AE and it can not fully block pathological progression.
