碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量和甲状腺球蛋白免疫诱发NOD小鼠甲状腺炎的病变特征

Objective To observe the pathological characteristics of thyroiditis induced by iodine excess and thyroglobulin (Tg) immunization and to explore the mechanism of thyroiditis induced by iodine excess. Methods NOD mice were used for intaking 0.05% Nal water and(or) Tg immunization. Morphologic change in thyroid and apoptosis were observed. The levels of serum TT4, TSH, thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) were measured. Responding to Tg, lymphocytic proliferation of lymph node and spleen, interleukin-4(IL-4)and γ-interferon(IFN-γ) levels in culture medium of splenocytes were detected. Real-time PCR Was used to detect mRNA expressions of IL-4, IFN-γ, chemokine ligand 10 (CXCL10) and intercellular adhesion molecular-1(ICAM-1) in thyroid. Results Distended thyroid follicles,colloid accumulation, intense lymphocytic infiltration and disorganization were seen in thyroid of iodine excess group, along with increased apoptosis of thyroid cells(34.66～ 2.78 vs 5.11±0.62 ,P<0.01). The levels of TT4 were lowered while TSH raised ,but no production of thyroid-specific autoantibodies was revealed. Lymph node and spleen cells showed positive respornse under stimulation of Tg. The level of IFN-γ[(1. 272±0.049 vs 1. 139±0. 025)ng/L,P<0. 01] was raised in culture medium of splenocytes but not IL-4. The expression of IFN-γ, CXCLI0 and ICAM-1 mRNA were increased in thyroid. But in Tg group, some lymphocytes were scattered in thyroid, autoantibodies emerged ,and the level of IL-4 was increased in cuhure medium of splenocytes[(18. 508±0. 113 vs 13. 368±0. 016)ng/L, P<0. 01]. ledine excess combined with Tg enhanced these inflammatory reaction. Conclusion Iodine excess induced thyroiditis in NOD mice. The process seems to be Th1 response dominant organ-specific autoimmune diseases. Iodine excess and Tg immunizatiou play a synergistic role in inducing experimental autoimmune thyroiditis.     

碘过量和甲状腺球蛋白免疫诱发NOD小鼠甲状腺炎的病变特征

Objective To observe the pathological characteristics of thyroiditis induced by iodine excess and thyroglobulin (Tg) immunization and to explore the mechanism of thyroiditis induced by iodine excess. Methods NOD mice were used for intaking 0.05% Nal water and(or) Tg immunization. Morphologic change in thyroid and apoptosis were observed. The levels of serum TT4, TSH, thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) were measured. Responding to Tg, lymphocytic proliferation of lymph node and spleen, interleukin-4(IL-4)and γ-interferon(IFN-γ) levels in culture medium of splenocytes were detected. Real-time PCR Was used to detect mRNA expressions of IL-4, IFN-γ, chemokine ligand 10 (CXCL10) and intercellular adhesion molecular-1(ICAM-1) in thyroid. Results Distended thyroid follicles,colloid accumulation, intense lymphocytic infiltration and disorganization were seen in thyroid of iodine excess group, along with increased apoptosis of thyroid cells(34.66～ 2.78 vs 5.11±0.62 ,P<0.01). The levels of TT4 were lowered while TSH raised ,but no production of thyroid-specific autoantibodies was revealed. Lymph node and spleen cells showed positive respornse under stimulation of Tg. The level of IFN-γ[(1. 272±0.049 vs 1. 139±0. 025)ng/L,P<0. 01] was raised in culture medium of splenocytes but not IL-4. The expression of IFN-γ, CXCLI0 and ICAM-1 mRNA were increased in thyroid. But in Tg group, some lymphocytes were scattered in thyroid, autoantibodies emerged ,and the level of IL-4 was increased in cuhure medium of splenocytes[(18. 508±0. 113 vs 13. 368±0. 016)ng/L, P<0. 01]. ledine excess combined with Tg enhanced these inflammatory reaction. Conclusion Iodine excess induced thyroiditis in NOD mice. The process seems to be Th1 response dominant organ-specific autoimmune diseases. Iodine excess and Tg immunizatiou play a synergistic role in inducing experimental autoimmune thyroiditis.     

胰岛素依赖型糖尿病的甲状腺功能及甲状腺自身抗体的测定

胰岛素依赖型糖尿病9/20并有低T_3,而T_4、TSH相对正常,1/20抗甲状腺球蛋白自身抗体阳性,6/20抗甲状腺微粒体自身抗体阳性,提示糖尿病可从下丘脑及外周组织T_4转换为T_3水平上影响甲状腺功能,且糖尿病可与其它内分泌靶腺特异或非特异器官的自身免疫性疾病同时存在。甲状腺功能的测定亦可作为对糖尿病病情估计、预后判定、疗效观察的辅助指标。甲状腺功能改变似与糖尿病病程有关     

16例ANCA相关性血管炎肺出血临床分析

目的回顾性分析抗中性粒细胞胞浆抗体(Antineutrophil cytoplasmic antibody,ANCA)相关性血管炎(ANCA-associated vasculitis,AAV)肺出血的临床特点、治疗及转归情况。方法收集2015年1月至2018年7月三峡大学第一临床医学院AAV肺出血患者16例,分析其临床表现、实验室检查结果、肺部影像学表现、治疗经过及转归。结果①AAV肺出血常见临床表现为咯血(62.5%),水肿(62.5%),胸闷、呼吸困难(56.25%)及咳嗽咳痰(50%);②所有患者有不同程度贫血,93.75%患者血肌酐升高,所有患者存在临床蛋白尿(24小时尿蛋白定量0.3g/24h);③MPO-ANCA阳性15例(93.75%),1例ANCA阴性(6.25%);④肺出血CT主要表现为肺实变、磨玻璃样变及斑片渗出影,8例(50%)肺部感染,7例(43.75%)纤维增殖灶,5例(31.25%)出现间质性肺炎,胸腔积液15例(93.75%);⑤5例患者因呼吸衰竭死亡,死亡率31.25%,死亡组入院时血肌酐值、血沉均显著高于存活组(P0.05),尿素氮、血红蛋白、C反应蛋白及白细胞值无显著性差异。⑥采用0.5g/d甲强龙冲击,联合环磷酰胺药物治疗6例,缓解率66.67%,死亡率33.3%,单纯使用40mg/d甲强龙药物治疗5例,缓解率60%,死亡率40%。结论 AAV肺出血急性发作病情进展极快,临床症状多样,多伴肾脏损伤,死亡率较高,治疗时需严密监测各项生化指标、肺部影像学动态变化,对判断病情进展有重要作用。