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Objective:To evaluate associations of psoriasis with adverse pregnancy outcomes.Methods:Databases, including CNKI, Wanfang, VIP, PubMed, Embase and Cohrane Library databases, were searched for published articles on associations between psoriasis and adverse pregnancy outcomes between January 1980 and December 2018. Quality of included articles was assessed by using MOOSE checklist. Statistical analysis was carried out with Review Manager 5.3 software.Results:One cohort study, 4 case-control studies and 2 cross-sectional studies meet the inclusion criteria. After heterogeneity test, meta-analysis was carried out by using a random effect model. The risks of cesarean ( OR= 1.17, 95% CI: 1.01- 1.37) , eclampsia or preeclampsia ( OR= 1.34, 95% CI: 1.00- 1.79) and premature birth ( OR= 1.09, 95% CI: 1.00- 1.19) were significantly higher in patients with psoriasis than in individuals without psoriasis (all P < 0.05) . There was no significant difference between patients with psoriasis and individuals without psoriasis in the risks of spontaneous abortion, low birth weight, high birth weight, stillbirth, congenital malformation, placental abruption, overdue delivery, low Apgar score (< 7) , polyhydramnios and oligohydramnios. Conclusion:The risks of cesarean, eclampsia or preeclampsia, and premature birth are higher in patients with psoriasis than in individuals without psoriasis.
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Obesity is a health problem of great concern to the whole society. Numerous studies have shown that obesity can lead to changes in the types and numbers of immune cell subsets and immune molecules in visceral adipose tissues, and IL-33/ST2 plays a crucial role in maintaining immune homeostasis. This paper reviewed the regulatory effects of IL-33/ST2 on adipocytes and immune cells in adipose tissues, as well as the changes of IL-33 in adipose tissues and the whole body during obesity in recent years.
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Obesity is a health problem of great concern to the whole society. Numerous studies have shown that obesity can lead to changes in the types and numbers of immune cell subsets and immune molecules in visceral adipose tissues, and IL-33/ST2 plays a crucial role in maintaining immune homeosta-sis. This paper reviewed the regulatory effects of IL-33/ST2 on adipocytes and immune cells in adipose tis-sues, as well as the changes of IL-33 in adipose tissues and the whole body during obesity in recent years.
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Objective:To investigate the effects of TLR4 knockout on immune cells and adipokines in mouse visceral adipose tissue.Methods: Cells were isolated from the spleen and epididymal adipose tissue of 20-week-old male wild type mice C57BL/6 and TLR4-/-.The expression of F4/80,CD11b,CD11c,CD3,CD4 and CD8 in these cells were analyzed by flow cytometry.The expression of IL-6,HMGB1,TNF-α,adiponectin and resistin in epididymal adipose tissue were detected by qPCR.Results: Compared with wild type C57BL/6 mice,the percentage of M1 macrophage which marked F4/80+CD11b+CD11c+ in spleen and epididymal adipose tissue of TLR4-/-mice increased(P<0.05) greatly,while that of M2 macrophage which marked F4/80+CD11b+CD11c-was decreased(P<0.05)significantly.This trend was more remarkable in epididymal adipose tissue than in spleen(P<0.05).In epididymal adipose tissue,the percentage of CD4+T cells decreased but that of CD8+T cells increased in TLR4-/-mice.Moreover,the high-level expressions of IL-6,HMGB1,resistin were found in epididymal adipose tissue of TLR4-/-mice.However,the expressions of TNF-α and adiponectin decreased obviously.Conclusion: TLR4 knock-out could lead to a disorder in adipokine and immune cells in visceral adipose tissue.
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Inflammation is part of the body′s response to invading pathogens and a crucial process in the maintenance of homeostasis .A variety of regulatory mechanisms are involved in inflammation process to limit the damage caused by excessive immune response to the host .Previous studies have shown that insu-lin resistance , type 2 diabetes , liver fibrosis and cardiovascular disease are caused by persistent chronic in-flammation in metabolic tissue (brain, fat, liver, pancreas, etc), especially in adipose tissue.However, the underlying mechanisms of these conditions have not been fully understood .The role of innate and adap-tive immune cells in these diseases attracts increasing attention .In this review, we will focus on the role of various immune cells in adipose tissue in the initiation and development of inflammation and discuss the effi -cacy of potential anti-inflammatory therapies based on their mechanisms .
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Objective To evaluate effects of ursolic acid (UA) on interleukin?33 (IL?33) expression in HaCaT cells induced by interferon?γ(IFN?γ), and to explore their mechanism. Methods Some HaCaT cells were treated with UA at different concentrations(0, 0.1, 1, 5, 10, 20, 40 and 80μmol/L)for 24, 48 and 72 hours separately. Then, methyl thiazolyl tetrazolium(MTT)assay was conducted to evaluate cell proliferative activity. A cell model of inflammation was established by culture of HaCaT cells with the presence of 200μg/L IFN?γ. Some HaCaT cells were classified into several groups to be treated with IFN?γ(200μg/L)and UA(10 and 15μmol/L)alone or in combination (firstly treated with IFN?γ followed by UA treatment), and those receiving no treatment served as the blank control group. Reverse transcription PCR (RT?PCR) was performed to detect mRNA expressions of IL?6 and IL?33, and Western?blot analysis to measure IL?33 protein expression after 12?hour culture. The expressions of extracelluar signal?regulated kinase 1/2(ERK1/2)and phosphorylated ERK1/2(p?ERK1/2)were also measured by Western?blot analysis after 5?and 60?minute treatments with IFN?γand UA alone or in combination. Results MTT assay showed that the treatments with 5-20μmol/L UA for 24 hours had no effects on cell proliferative activity, while 40-80μmol/L UA could significantly inhibit it at 24, 48 and 72 hours (all P 0.05), while IL?33 protein expression was significantly lower in the IFN?γ+15?μmol/L UA group than in the IFN?γ+10?μmol/L UA group(P<0.05). The p?ERK1/2 protein expression significantly increased in HaCaT cells treated with IFN?γ for 5 and 60 minutes compared with the blank control group, but significantly decreased in the IFN?γ+15?μmol/L UA group compared with the IFN?γgroup(0.458 ± 0.053 vs. 0.941 ± 0.042 at 5 minutes, 0.302 ± 0.054 vs. 0.509 ± 0.032 at 60 minutes, both P < 0.05). However, no significant differences were observed in the total ERK1/2 protein expression between the IFN?γ+15?μmol/L UA group and IFN?γgroup at 5 or 60 minutes. Conclusion UA can suppress IL?33 expression in HaCaT cells induced by IFN?γ, likely by regulating expressions of the ERK signaling pathway?related proteins.
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Objective:To study the effects of obesity induced by high-fat diet on T lymphocyte subsets in the adipose tissue in mice.Methods:C57BL/6 male mice were randomly divided into 2 groups, the normal control group and high-fat diet group.After feeding 16 weeks, serum was separated and CHOL, TG, HDL, LDL and glucose levels were measured by automatic biochemical analyzer.The concentrations of TNF-αwere determined by ELISA kit.FACS was used to analyze the number of T cells and the percentage of subgroup in epididymal fat adipose tissue.Results:Compared with control group,body weight,weight gain,epididymal fat pad weight,perirenal fat weight,blood lipids,glucose and TNF-αwere significantly increased in high-fat diet group,but there were no difference in the thymus index and spleen index between the two groups.Compared with the control group,the mice fed a high-fat diet had increasing proportion of CD3+T cells,CD4+T cells and CD8+T cells in adipose tissue and there was a significant increase on the proportion of Th1 and Th17 sublineage in the HFD group.Conclusion:High-fat diet induced obesity can lead to the increasing proportion of CD3+T cells,CD4+T cells and CD8+T cells in epididymal fat pads and generate a progressive Th1 and Th17 bias.
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Objective To explore the expression of early growth response gene-1 (EGR-1) in T cells that were positive for Tax protein of human T-cell leukemia virus type 1 (HTLV-1) and its possible reg-ulatory mechanism .Methods A series of expression structures carrying the regulatory elements of EGR-1 in different length and luciferase reporter genes were constructed .TaxP cells were transfected with the con-structs containing reporter genes and cultured with 5μmol/L of NF-κB inhibitor BAY 11-7082 or equal vol-ume of DMSO.After cultured for 24 hours the cells were collected to test the luciferase activity .BAY 11-7082 or equal volume of DMSO was added into the supernatant of TaxP cell culture to test the expression of EGR-1 protein by Western blot after 24 hours of culture .Tax and its mutants M22 and M47 were transfected into 293 T cells respectively to test the expression of EGR-1 protein by Western blot after 24 hours of culture . Results The expression structures carrying the regulatory elements of EGR-1 in different length and their mutants followed by luciferase reporter genes were successfully constructed .The luciferase activity in the cells transfected with the constructs containing the elements E 1 and E2 were higher than that transfected with E3, DelE and MutE, but the reporter gene expressions were decreased with the interference of BAY 11-7082 (P<0.01).However, there were no significant changes with the luciferase activity in the cells transfected by elements E3, DelE and MutE.Western blot analysis indicated that the expression of EGR-1 protein was significantly decreased with the interference of BAY 10-7082 .The expression of EGR-1 protein in M22 mu-tants-transfected 293 T cells were decreased significantly in comparison with those by wild type tax-and M47-transfected cells .Conclusion NF-κB was the key nuclear factor in regulating the expression of EGR-1 pro-tein in Tax-positive T cells .
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Objective To investigate the influence of extracellular high mobility group box 1 (HMGB1) on viral replication in HTLV-1 infected T cells.Methods HMGB1 in culture supernatants of adult T-cell leukemia virus 1 (HTLV-1) virus-negative cell:Jurkat,MOLT4 cells and HTLV-1 virus-positive cells:MT2,MT4,was detected by ELISA;The HTLV-1 long terminal repeat reporter gene (pHTLV-1-LTR-luc) was transfected into MT2 cells by Tfx-50-mediated transfection,and 0.25,0.50,0.75 μg/ml of HMGB1 polyclonal antibody(HMGB1 PcAb) and its isotype control rabbit IgG antibodies,0.03,0.1,0.3 μg/ml rhHMGB1 and its control PBS,were added into culture supernatant respectively,then luciferase activity was detected after 48 h;Similarly,0.25 μg/ml HMGB1 PcAb and the isotype control antibody,0.3 μg/ml rhH-MGB1 and the control PBS were added to the culture supernatant of MT2 cell,the viral gene,pol1,pol2,gag,env,etc,were performed by real-time PCR.Results Culture supernatant HMGB1 levels has no significant difference between HTLV-1 positive cells MT2 and MT4 and the other two virus-negative T cell lines;Compared with isotype control antibody group,the culture supernatant,to which is added 0.25 μg/ml HMGB1 PcAb,can significantly inhibit the HTLV-1-LTR transcriptional activity and suppress the expressions of the viral gene pol1,pol2,gag,env.Compared with the control PBS,0.3 μg/ml rhHMGB1 significantly promotes the transcriptional activity of the HTLV-1-LTR and the expressions of the viral gene pol1,pol2,gag,env.Conclusion The extracellular HMGB1 can promote viral replication of HTLV-1 infected T cells.
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Objective To study the effects of the adult T cell leukemia virus type 1(HTLV-1) Tax protein on T lymphocytes self-reactive growth hormone(GH). Methods The expression of the growth hormone protein was measured by Western blot in TaxP and TaxN cells, which expresses HTLV-1 Tax or no. The location of growth hormone in the TaxP and TaxN cells were detected by LSCM(laser scanning confocal microscope). The level of growth hormone mRNA in TaxP and TaxN cells was measured by RT-PCR. The pGL2-GH-luc was transfected in TaxN and TaxP cells by Tfx-50-mediated transfection to assay transcriptional activity. The pNF-κB-luc, pAP-1-luc and pNFAT-luc was transfected into TaxP cells with pcDNA3.0-GH by Tfx50 to test bioactivity of the nuclear transcription factors. Results The mRNA and protein expression of GH could be promoted significantly by Tax. Relative to the TaxN cells, the transcriptional activity of GH was significantly increased about 6.37 times in TaxP cells(P＜0.05). Overexpression of GH can increase the activity of NF-κB about 1.7 times in TaxP cells (P＜0.05). Conclusion GH maybe involve in adult T-cell leukemia(ATL) through activating NF-κB.
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Objective To detect the FHIT gene promoter methylation and protein expression in mycosis fungoides(MF).Methods Tissue specimens were collected from 48 patients with MF and 18 normal human controls.FHIT protein expression was determined by immunohistochemistry,and methylation status of FHIT gene by methylation-specific PCR.Results Abnormal methylation of FHIT gene was found in 26(54.2%)out of the 48 specimens.Thirty(63.5%)specimens of MF were negative for FHIT protein,which was observed in all the control specimens.The promoter methylation of FHIT was closely correlated with the protein expression of FHIT,but unrelated to the sex of,tumor staging or lymph node metastasis in patients with MF.Conclusion The FHIT gene promoter methylation may contribute to the inactivation and abnormal expression of FHIT protein in MF.
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Objective To investigate the effect of the exogenous fragile hisdidine triad(FHIT) gene on the proliferation and the apoptosis of cutaneous carcinoma cell line A431,and to explore the mechanism of tumor suppression by the FHIT gene.Methods The plasmids pcDNA3-FHIT and pcDNA3-vector were transfected into the cutaneous carcinoma cell line A431 without FHIT gene expression,and then the transfected cells were screened by G418 and the expression of FHIT was determined by the immunocytochemical staining technique.The effect of FHIT on the growth characteristics of cutaneous carcinoma cell line A431 was observed by MTT,colony forming test and flow cytometry.Results Stable FHIT gene expressing A431 cells were produced,the proliferation activity and colony forming capability of A431FHIT were suppressed,whereas the apoptosis was increased.All these differences between A431-FHIT cells and the two control groups of cutaneous carcinoma cells had statistical significance.Conclusion Transfecting the exogenous FHIT gene into cutaneous carcinoma cells line A431can suppress the proliferation of tumor cells,and can also induce apoptosis and cell cycle arrest.
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The exprimental teaching of medical immunology is the important constituent.We have explored the existing problems on course content,teaching method and experimental test way according to our practical teaching experience for the past few years.We have also made the preliminary attempt about reforming exprimental teaching of medical immunology.
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BACKGROUND: Cristata L flavonoid is a kind of plant estrin, which possesses multiple physiological function, has no toxicity and adverse effect, and is effective in treating and preventing osteoporosis.OBJECTIVE: To study the effect of cristata L flavonoid on bone morphogenetic protein, urine inorganic salt and content of lysozyme of rats with diabetes mellitus (DM).DESIGN: Randomized grouping design and controlled study.SETTING: Pharmaceutical Laboratory of Xinxiang Medical College.MATERIALS: The experiment was completed in the Xinxiang Medical College from September to December 2003. Totally 24 health male SD rats were randomly divided into three groups: normal control group, diabetes mellitus (DM) group, DM + cristata L flavonoid group with 8 in each group.were injected intraperineally with 60 mg/kg streptozotocin, and 48-72 hours later, blood of rear caudal vein was collected to measure total blood glucose.Rats were determined as DM if the blood glucose was ≥ 16.7 mmol/L; oth erwise, 60 mg/kg streptozotocin was injected once more. After modeling,cristata L flavonoid and rats in normal control group were given the same was measured with atomic absorbency method and content of urine sodium histochemistry of bone morphogenic protein-2 (BMP2) in bone was detected with streptavidin tagged by peroxidase and immunohistochemic expression lysozyme reflected reabsorption function of renal tubule was measured with with t-test. MAIN OUTCOME MEASURES: Comparison between content of calcium, sodium, kalium in urine and lysozyme and immunohistochemic expression of BMP2 10-week intervention later.calcium and sodium in urine in DM model group were obviously higher than those in normal control group, but content of kalium in urine was obviously lower (P ＜ 0.05-0.01). Contents of calcium in urine in DM +cristata L flavonoid group were obvioualy lower than those in DM model group and normal control group were obviously higher than those in DM model group, and content of lysozyme in urine in those groups was obviously lower than that in DM model group (P ＜ 0.05-0.01).CONCLUSION: Expression of BMP2 of DM rats is decreased, but after supplement of cristata L flavonoid compound, the expression is increased.In addition, output of urine calcium and sodium in DM rats is decreased,and reabsorption function of renal tubule is increased.
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Objective To construct eukaryotic cell expression vector of human frangible histone triad (FHIT) gene. Methods A 456 bp cDNA fragment was amplified from the total RNA of normal human thyroid tissue by RT PCR method and cloned into plasmid pcDNA3. The cloned insert was identified by double digestion of the recombinant plasmid with restriction enzymes Kpn Ⅰ and Bst XⅠ and sequenced by Sanger dideoxy mediated chain termination. The expression of FHIT gene was detected by immunocytochemical methods. Results The results showed that the cDNA fragment included 456 bp entire coding region. The recombinant eukaryotic cell expression vector of pcDNA3 FHIT was constructed, and the sequence of the insert was identical to the published sequence. MM96L cells transfected with the pcDNA3 FHIT plasmid expressed high level of Fhit protein in cytoplasm. Conclusion The recombinant plasmid pcDNA3 FHIT can provide a strong molecular tool for the studies of neoplasm pathogenesis.