白术多糖对小鼠淋巴细胞功能的调节

研究了白术多糖ＰＡＭ体内及体外对小鼠脾淋巴细胞的调节作用。结果表明：白术多糖ＰＡＭ在一定的浓度范围内能单独激活或协同ＣｏｎＡ／ＰＨＡ促进正常小鼠淋巴细胞转化并能明显提高ＩＬ－２分泌的水平。ＰＡＭ对氢化可的松造成的免疫抑制小鼠淋巴细胞的增殖功能有恢复作用。同时还发现白术多糖ＰＡＭ对淋巴细胞的调节与β－肾上腺素受体激动剂异丙肾上腺素相关。     

中枢IL-2对脾脏免疫机能的调节

研究了大鼠第三脑室注射白细胞介素２（Ｉｎｔｅｒｌｅｕｋｉｎ２，ＩＬ－２）对脾淋巴细胞增殖功能的影响。结果显示，第三脑室注射ＩＬ－２可引起脾淋巴细胞对植物血凝素刺激引起的增殖作用的增强，同时还引起脾交感神经活动的抑制。ＩＬ－２的这些作用均可被阿片受体阻断剂纳洛酮阻断。实验还发现，电刺激脾神经可以引起脾淋巴细胞增殖功能的抑制。根据结果可以认为脑室注射ＩＬ－２可以通过阿片受体介导的途径抑制交感神经的活动，进而通过脾交感神经影响脾淋巴细胞增殖     

鱼王浆对免疫功能低下小鼠IL-2、IL-6及溶血素、溶血空斑的影响

目的研究鱼王浆对免疫功能低下小鼠相关细胞因子IL-2、IL-6及溶血素、溶血空斑的影响和量效关系。方法通过环磷酰胺注射制造模型小鼠,比较鱼王浆各剂量对免疫功能低下小鼠相关免疫细胞因子的影响,采用ELISA法检测IL-2及IL-6含量的变化,以鸡红细胞为抗原的溶血素及溶血空斑的测定。结果鱼王浆高、中治疗组IL-2、IL-6的含量明显高于模型组;鱼王浆各治疗组溶血素及溶血空斑的含量明显高于模型组。结论鱼王浆能明显提高免疫功能低下模型小鼠外周血中相关免疫细胞因子IL-2、IL-6的含量,促进溶血素及溶血空斑的生成,并且其作用具有明显的量效关系。     

吗啡对小鼠的细胞免疫调节

目的：动态观察吗啡对小鼠免疫功能的影响。方法：制作吗啡急性作用和吗啡依赖小鼠模型，以盐水及空白组为对照。分离单个核细胞，用间接免疫荧光检测Ｔ细胞亚群，加ＣｏｎＡ、ＬＰＳ进行２４小时培养，检测上清中ＩＬ－６、ＩＬ－２、ＮＯ水平。结果：注射吗啡（８０ｍｇ／ｋｇ／ｄ）７天后出现淋巴器官重量的减轻，Ｔ细胞亚群的改变，细胞因子ＩＬ－６显著升高，ＩＬ－２显著降低，ＮＯ水平在注射吗啡１、３、５天时显著升高。结论：吗啡可抑制小鼠的免疫功能，ＴＨ１细胞和ＴＨ２细胞的功能失衡可能是吗啡影响免疫系统的一个中介因素。     

人胎脾LAK细胞活性发育动力学

本文采用4h~(51)Cr释放试验观察了不同眙龄脾的LAK细胞活性。胚胎发育至16周时,胎脾淋巴细胞经IL-2诱导72～96h后,产生明显的LAK活性,对Raji靶细胞的杀伤率为67.7±2.2％,而16周前(15周)的LAK活性低下(20.2±5.8％)。结果还显示,16周后的胎睥LAK活性与眙龄增长无关,与正常成人水平无显著性差异(P>0.05);胎脾LAK前体细胞的发生可能早于NK细胞。     

甲状腺激素对小鼠脾淋巴细胞增殖反应和IL-2生成的影响

给小鼠用丙基硫氧嘧啶(PTU)抑制其体内甲状腺激素的合成以制备实验性“甲低”小鼠模型。该鼠脾淋巴细胞的增殖反应及白细胞介素II(IL-2)的生成均明显低于对照小鼠,给“甲低”小鼠补充不同剂量的L-T_4后,其脾淋巴细胞增殖反应随血中T_3、T_4水平的恢复呈剂量依赖性增强,当剂量过大(10mg/kg)时,血中T_3、T_4含量明显高于正常,此时,脾淋巴细胞增殖反应反而下降。将正常小鼠的脾淋巴细胞在体外培养,加入L-T_2(10~(14)～10~(-6)或L-T_4(10~(-12)～10~(-4)均可剂量依赖性地促进ConA诱导的脾淋巴细胞增殖,分别在10~(-10)M及10~(-2)M时达最大效应,剂量进一步增加,增殖反应反而下降,这与体内实验结果基本一致。在加了L-T_4且经48小时培养的脾淋巴细胞上清液中未检出T_3,表明L-_4不需转变为T_3即可发挥作用,即T_3、T_4均能直接影响脾淋巴细胞的增殖。本实验结果证明甲状腺激素在体内外均能促进T淋巴细胞增殖,其机制与促进IL-2生成有关。     

人rIL-6对人胎脾单个核细胞IL-2合成的影响

用人重组白细胞介素6与人胎脾单个核细胞(FSMC)共同培养24小时,结果发现其培养上清含有明显的IL-2活性,与对照组相比,差异有非常显著性(P<0.0001),且IL-2产生与IL-6刺激剂量呈依赖关系;不同胎龄FSMC经相同剂量IL-6处理后产生的IL-2水平差异无显著性(P>0.05)。结果提示IL-6能诱导FSMC产生IL-2。     

硒酸精氨酸对D-gal衰老小鼠细胞免疫功能的影响

目的：探讨硒酸精氨酸对D-gal衰老小鼠免疫功能的影响。方法：将试验小鼠分为正常组、模型组、低剂量给硒组（L-SeArg）和高剂量给硒组（H-SeArg），通过后颈背部皮下注射D-gal建立亚急性衰老模型，以灌胃方式加入硒酸精氨酸，观察硒酸精氨酸对脾指数、胸腺指数的影响，MTT法检测脾细胞增殖能力和NK细胞的杀伤活性、免疫荧光法观察CD40、CD40L的阳性表达率。结果：硒酸精氨酸能明显提高小鼠胸腺指数和脾指数，促进淋巴细胞转化，提高NK细胞的杀伤活性，增加CIM0、CD40L的阳性表达率。2个剂量给硒组中，低剂量硒酸精氨酸的影响最大，与模型组相比有统计学意义（P〈0．01）。结论：D-gal能导致小鼠细胞免疫功能下降，硒酸精氨酸能活化免疫细胞，提高小鼠机体的免疫力，延缓衰老。     

IL-2对荷瘤小鼠红细胞免疫粘附功能及抑瘤生长的研究

ＩＬ-２对荷瘤小鼠红细胞免疫粘附功能及抑瘤生长的研究曹卉，明建扩，吕厚东（济宁医学院微生物学教研究室济宁２７２１１３）柳青，曹蕊（济宁肿瘤医院放疗科济宁２７２１０３）近几年的研究表明，白细胞介素２（ＩＬ-２）对红细胞免疫功能也有提高作用［１￣３］。本文...     

枸杞多糖对糖尿病小鼠模型免疫功能的影响

利用静脉注射四氧嘧啶 ( 10 0mg/kg)诱导制备糖尿病小鼠模型 ,观察LBP D对四氧嘧啶致糖尿病小鼠免疫功能的影响。研究表明 ,小鼠在注射四氧嘧啶后 72h ,灌胃 (ig )给予LBP D ,连续 10d ,糖尿病小鼠NS对照组免疫功能明显降低 ,而LBP D组显示LBP D具有明显促进小鼠淋巴细胞增殖、调节T淋巴细胞亚群及提高IL 1和IL 2水平的功能 ,使四氧嘧啶糖尿病小鼠免疫功能恢复接近正常。研究结果显示 ,LBP D对糖尿病模型小鼠有免疫调节治疗效应     

吗啡对小鼠巨噬细胞吞噬,细胞毒作用及诱生细胞因子的影响

小鼠递增剂量ｓｃ给予吗啡共４天，可建立稳定的躯体依赖模型。急性吗啡依赖使小鼠腹腔巨噬细胞（Ｍφ）吞噬中性红能力降低；使其对Ｓ１８０肿瘤细胞的细胞毒作用减弱；并平行性地抑制脂多糖（ＬＰＳ）诱导的白细胞介素１（ＩＬ－１）和肿瘤坏死因子（ＴＮＦ）的产生及其活性，纳洛酮可拮抗吗啡所致Ｍφ的功能抑制，而其单独给药对Ｍφ功能无明显影响。结果提示Ｍφ在阿片滥用所致免疫抑制的重要作用，且其体内效应可能通过阿片受体     

狼疮性BXSB小鼠脾脏淋巴细胞增殖与凋亡的初步分析

为了比较全面准确地了解系统性红斑狼疮 (SLE )BXSB小鼠的发病过程中 ,淋巴细胞增殖与凋亡的动力学变化及其机制。采用细胞双色荧光染色的标记技术 ,检测了脾脏淋巴细胞中的增殖细胞和凋亡细胞的百分率 ,并且测定了巨噬细胞吞噬凋亡细胞的能力。结果发现 ,发病的雄性BXSB小鼠和雌性BXSB小鼠脾脏中增殖的CD4 + T淋巴细胞和B淋巴细胞百分率显著高于对照C5 7小鼠 ,而凋亡的B淋巴细胞的百分率显著低于对照C5 7小鼠 ;但是 ,雌雄BXSB小鼠和对照C5 7小鼠巨噬细胞吞噬凋亡细胞的吞噬指数相同。本研究结果表明 ,在BXSB小鼠的SLE发病过程中 ,淋巴细胞的增殖速度异常升高、而凋亡速度下降 ,可能与其脾脏肿大有关 ;而且淋巴细胞的增殖与凋亡的失衡与巨噬细胞的功能无关 ,可能与淋巴细胞内在的异常有关。     

Effect of Sympathetic Nerves on Proliferation of Splenic Lymphocytes and Antioxidant Function of Maternal Spleen in Early Pregnant Mice

Sympathetic regulation plays an important role in fetal survival and development during early pregnancy. Maternal adaptations to pregnancy may involve changes of the spleen in its structure, size, and function. This study was therefore designed to investigate the effects of sympathetic nerves on these adaptations in the maternal spleen of mice during early pregnancy. The adult female mice were intraperitoneally injected with neurotoxin 6‐hydroxydopamine (6‐OHDA) for 5 consecutive days to selectively destroy the sympathetic nerves. The results were as follows: (1) the splenic weight was reduced in the 6‐OHDA group by 10.9%–13.0% at E5–E9 (P < 0.05) when compared with the control group. (2) The splenic nodule and periarterial lymphatic sheath of the 6‐OHDA‐treated mice were smaller than those of control mice. The proliferating cell nuclear antigen positive cells of 6‐OHDA‐treated group were decreased by 10.9%–16.2% (P < 0.05) at E1–E9. (3) Lymphocyte proliferation indices in response to concanavalin A or lipopolysaccharide were significantly decreased (P < 0.05) in the 6‐OHDA group. (4) When compared with control mice, the superoxide dismutase and glutathione peroxidase activities of 6‐OHDA‐treated mice were decreased by 14.3%–21.9% (P < 0.05) at E1–E9 and 17.4%–25.0% (P < 0.05) at E3–E9, respectively. In contrast, the malondialdehyde content of 6‐OHDA group was increased by 10.6%–38.6% (P < 0.05) at E3–E9. The results demonstrated the regulation of pregnancy‐dependent adaptations in the spleen through the sympathetic nerve activity. Anat Rec,, 2011. © 2011 Wiley‐Liss, Inc.     

Immunoprotective Effects of Prolactin during Stress-Induced Immune Dysfunction

We showed for the first time that prolactin stimulates the synthesis and release of immunomodulating cytokines and lymphocyte-activating factors (e.g., interleukin-1) by peritoneal macrophages. Prolactin abolished the stress-induced inhibition of proliferation of peripheral blood lymphocytes and increased cell sensitivity to regulatory effects of interleukin-1 in the reaction of lymphocyte blast transformation. These data illustrate the mechanism of immunoprotective activity of prolactin during stress.     

Behavioral and Immune Changes in V-Ha-ras Transgenic Mice

Abstract

Transgenic mice (Oncomice) with an activated v-Ha-ras oncogene under the control of the mouse mammary tumor virus promoter develop mammary tumors. We wondered if the expression of the v-Ha-ras oncogene product would induce changes in mice behavioral activity, that could be associated with alterations in their immune system. Behavior was evaluated in an open field study considering line crossings and rears. Oncomice consistently showed less activity than FVB mice. Lieber-DeCarli diet decreased both types of activity in both strains. Cocaine treatment increased line crossings in both strains. Oncomice spleen and thymus cell supernatants contained higher levels of IL-2. Oncomice serum had higher levels of IL-1α. Our results suggest a direct association between higher levels of IL-1α and lower open field activity. Therefore, we can infer that the increased level of IL-1α found in Oncomice, could have a key role in oncogene induced immune and behavioral changes, and could be a requirement to facilitate its transforming activity.     

氯苯丙氨酸对褪黑素免疫调节作用的影响

本文研究了5-羟色胺（5-HT）合成抑制剂对氯苯丙氨酸（PCPA）对褪黑素（MT）免疫调节作用的影响。结果表明,MT20μg/kg可以显著升高小鼠外周血淋巴细胞百分率（Lym％）、T-淋巴细胞百分率（T-Lym％）与血清溶血素生成水平（半数溶血值,HC_(50)值）,PCPA 10～40mg/kg本身对小鼠Lym％、T-Lym％及HC_(50)基本无影响,但可完全抑制MT升高Lym％、T-Lym％与HC_(50)值的作用,提示MT的免疫调节作用机制之一可能与5-HT介导有关。     

人甲胎蛋白对荷H-22肝癌小鼠免疫功能的影响

作者通过体外实验观察人甲胎蛋白(AFP)对荷H-22肝癌小鼠免疫功能的影响.结果表明,人AFP抑制单向混合淋巴细胞反应和白介素6的生成,并促进抑制性T细胞的诱生.     

Morphine modulation of the contact hypersensitivity response: characterization of immunological changes

Previous investigations in our laboratory showed that systemic morphine administration 1 h prior to elicitation of the in vivo contact hypersensitivity (CHS) response produced a robust increase in inflammation at the site of antigen reexposure. The present study extended those findings by characterizing the effect of morphine on immunological processes important in the development of the CHS response. To induce contact hypersensitivity, the antigen 2,4-dinitrofluorobenzene was applied to the pinnae of previously sensitized rats. Morphine administration produced an increase in inducible nitric oxide synthase mRNA and the proinflammatory cytokine interleukin-6, at the site of antigen reexposure. In contrast, morphine did not alter expression of the anti-inflammatory cytokine interleukin-10. Morphine also produced an increase in the proliferation of lymphocytes from the peripheral (i.e., cervical) lymph nodes when assessed 72 h following challenge. These studies show that the morphine-induced increase in the in vivo CHS response involves immunologically specific alterations.