Gestational vitamin A deficiency reduces the intestinal immune response by decreasing the number of immune cells in rat offspring

ObjectivesVitamin A (VA) is a critical micronutrient for life, especially during growth and development. There is a close relationship between VA deficiency (VAD) and the morbidity of diarrhea in the clinical setting. However, the regulatory mechanisms of VA are not clearly understood.MethodsSpecific-pathogen–free Wistar rats received a diet with or without VA before gestation. The offspring were submitted to an abdominal injection of Escherichia coli lipopolysaccharide. After the challenge, which lasted for 12 h, the serum retinol was detected by high-performance liquid chromatography, and the level of immunoglobulin A in the stool was analyzed by enzyme-linked immunosorbent assay. The lymphocyte immunophenotypes were evaluated with the use of flow cytometry with samples collected from the spleen, the mesenteric lymph nodes, Peyer patches, and intestinal intraepithelial lymphocytes.ResultsEarly life VAD, independent of the lipopolysaccharide challenge, significantly decreased serum retinol level and CD8⁺ intestinal intraepithelial lymphocytes. The level of immunoglobulin A secretion and percentages of splenic CD4⁺CD8⁺ T cells were affected by the interaction effects of the lipopolysaccharide challenge and VAD treatment. Gestational VAD significantly increased the percentages of B cells in the mesenteric lymph nodes and decreased the percentages of CD11 _C⁺ dendritic cells and CD4⁺CD25⁺ T cells from the Peyer patches. The lipopolysaccharide challenge only significantly increased percentages of splenic CD4⁺CD25⁺ T cells. The intestinal tissue of the pups with VAD displayed mild inflammation.ConclusionsGestational or early life VAD decreases the numbers of immune cells in offspring, which may partly suppress the activities of the mucosal immune responses in the intestine. This suggests that more attention should be given to the VA nutritional state of children and women of reproductive age.     

免疫功能受损宿主外周血单个核细胞端粒酶活性研究

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双功能抗体介导胃癌杀伤效应的研究

目的 以化学方法将抗CD3及抗三硝基苯（TNP）的单克隆抗体（McAb)交联为双功能抗体。利用此双功能抗体介导人外周血淋巴细胞（PBLS）对于不同抗胃癌McAb所针对的胃癌细胞进行体内外杀伤试验。方法 利用化学交联法制备双功能抗体,以酶联免疫吸附试验(ELISA）测定McAbs活性,以ELISA桥联法、琼脂糖免疫双扩散及十二烷基磺酸钠－降丙烯酰胺凝胶电泳（SDS－PAGE）对于双功能抗体进行鉴定,以细胞杀伤试验及肿瘤生长抑制实验检测双功能抗体作用。结果 将抗CD3及抗TNP McAb交联为双功能抗体,此双功能抗体可介导PBLS对于不同抗胃癌McAb所针对的胃癌细胞进行体内外杀伤试验。结论 此双功能抗体在肿瘤生物免疫治疗中具有应用前景。     

老年小鼠淋巴结T淋巴细胞的功能变化

目的：探讨老年小鼠淋巴结T淋巴细胞的功能。方法：采用^3H-TdR掺入法测定淋巴细胞的增殖;^3H-缬氨酸掺入法测定总蛋白合成;以依赖株细胞增殖反应测定法检测IL－2活性;^3H-缬氨酸掺入IL－2单克隆抗体－IL－2复合物,检测IL－2蛋白合成能力。结果：20月龄老年小鼠和27月龄老年小鼠与4月龄青年小鼠相比,其淋巴结细胞的增殖能力分别下降65．6％和32．8％;总蛋白合成下降40．2％和48．9％;IL－2活性下降36．6％和71．5％;IL－2蛋白合成能力下降32．9％和57．1％。结论：老年小鼠淋巴结细胞对ConA刺激的增殖能力、总蛋白合成水平、IL－2活性及IL－2蛋白合成水平与青年小鼠相比显著下降。     

类风湿关节炎中HLA-DR分子表达量的改变

目的 探讨外周血淋巴细胞表面HLA－DR分子表达量在类风湿关节炎（RA）发病中的作用。方法 选择RA患者活动期34例,静止期40例;正常对照（NC）43例,急性风湿性关节炎（ARA）21例及系统性红斑狼疮（SLE）28例,分别检测外周血淋巴细胞表面的HLA－DR分子表达量。同时在活动期RA治疗3个月前后,分别检测HLA－DR分子表达量、类风湿因子（RF）及对症状计分,进行统计学分析。结果 ①RA活动组HLA－DR分子表达水平最高（P＜0．05）,ARA组及RA静止组较NC组明显增高（P＜0．05）,而SLE组与NC组无明显差别（P＞0．05）;②RA活动组HLA－DR分子表达量及RF的阳性率均在治疗后显著下降,临床症状明显改善。结论 ①检测患者外周血淋巴细胞表面HLA－DR表达量有助于RA的诊断及监测RA活动度;②HLA－DR分子表达量与RF的动态变化相平行;③动态观察HLA－DR分子表达量变化有助于判断RA病情及其预后。     

黄曲霉毒素G_1对体外培养HPBM增殖及TNF-α分泌的影响

目的 :研究黄曲霉毒素G1(AFG1)对体外培养人外周血单个核细胞 (HPBM)增殖及细胞TNF -α分泌的影响。方法 :采用流式细胞术 (FCM)和MTT比色法研究AFG1对HPBM增殖的影响。以双抗体夹心ELISA法检测AFG1对HPBMTNF -α分泌的影响。结果 :FCM检测结果显示 ,AFG1作用 6h ,10 0 0 μg/L处理组HPBM的增殖指数明显高于对照组。AFG1作用 2 4h ,2 0 0 μg/L和 10 0 0 μg/L浓度的AFG1可明显刺激HPBM增殖 ;回归分析结果表明 ,AFG1作用 6h和 2 4h ,AFG1浓度均与增殖指数呈正相关 (r分别为 0 5 12 2和 0 5 119,P均 <0 0 5 )。MTT比色法结果显示 ,2 0 0 0 μg/LAFG1处理HPBM的A值明显高于对照组。AFG1在 10 0 μg/L浓度下可显著抑制TNF -α分泌 (P <0 0 5 )。结论 :AFG1对体外培养HPBM的增殖有刺激作用 ,在 10 0 μg/L浓度下对HPBMTNF -α的分泌有一定抑制作用。     

颅内肿瘤淋巴细胞核仁区酸性非组蛋白的表达

目的探讨颅内肿瘤患者外周血T淋巴细胞银染核仁区酸性非组蛋白（Ag-NORs）表达特点。方法应用KL-2图像分析系统及其配套细胞培养银染等试剂和方法,分析47例颅内良性和恶性肿瘤患者外周血淋巴细胞Ag-NORs的表达,并与40名健康人和32例其他系统恶性肿瘤相比较。结果颅内良性肿瘤组患者Ag-NORs表达降低,平均值为（6.42±0.16）%,与健康人相比差异有非常显著意义;颅内恶性肿瘤组患者降低更明显［平均值(5.73±0.22)%］,与良性组相比差异有显著意义;其他系统恶性肿瘤组患者平均值［(3.68±0.19)%］比颅内恶性肿瘤组降低更加明显,差异有非常显著意义。结论外周血T淋巴细胞Ag-NORs可以作为标记颅内肿瘤的参考指标。颅内肿瘤患者的细胞免疫缺陷程度与其他系统肿瘤有差异。     

硒对提高胃肠癌患者术前免疫水平的探讨

本将３１例胃肠癌患分为治疗组和对照组（未加服硒），观察术前投药前后血清硒浓度与Ｔ淋巴细胞亚群、ＮＫ细胞的活性的变化。结果显示：胃肠癌患入院时血硒水平为０．８２５±０．１１μｍｏｌ／Ｌ，低于正常对照组，口服硒剂后血硒浓度升高，与对照组相比差异有显性，服硒后血中ＣＤ３、ＣＤ４、ＣＤ８细胞以及ＣＤ４／ＣＤ８细胞比值仍维持原有的水平，但对照组有所下降（Ｐ〈０．０５）〉值得注意的是服硒后患血中ＮＫ     

The Associations of Alcohol Drinking and Drinking Cessation to Measures of the Immune System in Middle-Aged Men

To estimate the association between the immunologic responses of the cell-mediated and humoral systems and alcohol drinking, we used data from the Vietnam Experience Study conducted by the Centers for Disease Control. That study, conducted from 1985 to 1986, was based on a random sample of 4462 male, Vietnam-era, U.S. veterans. By using linear regression, we evaluated how (1) the number of alcoholic drinks the subjects consumed per month and (2) the drinking cessation of certain subjects were associated with their relative and absolute T, B, CD4, and CD8 lymphocyte counts and immunoglobulin A (IgA), IgM, and IgG levels. We used geometric means and percentage differences in geometric means of immune status to measure the associations and adjusted these values to account for the effect of covariates. The results indicated that measures of immune status differed among the drinking categories and that, generally, the differences changed after adjustment for covariates. These differences consisted, as alcohol consumption increased, of higher IgA and IgM levels, relative T and CD4 lymphocytes, and the ratio of CD4 to CD8 cells, and of lower IgG levels, relative B and CD8 lymphocytes, absolute lymphocyte, and lymphocyte subset counts after adjusting for other covariates. Among former drinkers, we found no clear-cut pattern in measures of immunity for a few years after cessation and then found that values of former drinkers tended to return toward values of nondrinkers as they continued to abstain.     

氨茶碱及地塞米松对小鼠脾淋巴细胞凋亡的调节作用

目的：观察氨茶碱和地塞米松对小鼠脾淋巴细胞凋亡的调节作用。方法：采用流式细胞技术对比了它们对正常鼠及卵蛋白致敏小鼠脾淋巴细胞凋亡的作用。结果：氨茶碱及地塞米松可诱导体外培养的正常小鼠淋巴细胞凋亡，明显抑制体外培养的致敏鼠淋巴细胞的凋亡。致敏鼠淋巴细胞的凋亡明显多于对照鼠，在体应用氨茶碱（１００ｍｇ／ｋｇ）使致敏淋巴细胞凋亡进一步增加，而在体应用地塞米松（４０ｍｇ／ｋｇ）明显抑制致敏鼠淋巴细胞的凋亡。氨茶碱体外对在体应用氨茶碱处理的鼠淋巴细胞的凋亡有抑制作用，地塞米松体外对在体应用地塞米松处理的鼠淋巴细胞的凋亡无明显影响。结论：氨茶碱和地塞米松对淋巴细胞凋亡具有重要的调节作用，两者的作用机制可能有别。