胃溃灵对消化性溃疡患者免疫功能调节作用的探讨

从临床及动物实验角度，探讨胃地消化性溃疡患者免疫功能的调节作用。结果表明：溃疡患者胃液ＩｇＧ水平明显低于正常人，而ＳＩｇＡ明显高于正常人，经胃溃灵治疗后，消化性溃疡患者胃液中ＩｇＧ水平显著提高，ＳＩｇＡ水平明显降低，两者与正常人比较无显著性差异。实验结果，胃溃有明显提高小白鼠血清抗体效价，增加其血清溶菌酶含量，增强其单核巨噬细胞的吞噬功能。提示胃溃灵对机体免疫功能有良好的调节作用。     

胃溃灵对消化性溃疡患者免疫功能调节作用的探讨

从临床及动物实验角度，探讨胃溃灵对消化性溃疡患者免疫功能的调节作用。结果表明：溃疡患者胃液IgG水平明显低于正常人，而SIgA明显高于正常人，经胃溃灵治疗后，消化性溃疡患者胃液中IgG水平显著提高，SIgA水平显著降低，两者与正常人比较无显著性差异、实验结果，胃溃灵能明显提高小白鼠血清抗体效价，增加其血清溶菌酶含量，增强其单核巨噬细胞的吞噬功能。提示胃溃灵对机体免疫功能有良好的调节作用。     

肝康乐对免疫功能低下小鼠的免疫调节作用

目的探讨中药复方肝康乐对免疫抑制小鼠免疫功能的调节作用。方法通过给小鼠腹腔注射免疫抑制剂环磷酰胺复制免疫功能低下的动物模型,然后灌胃给予肝康乐高、中、低剂量,1次/d,连续10 d,分别测定小鼠的脾指数、胸腺指数,巨噬细胞的吞噬功能以及溶血素水平;二硝基氯苯诱导迟发型变态反应(DTH),观察肝康乐对DTH的影响。结果肝康乐能够显著提高免疫低下小鼠的碳粒廓清率、脾指数、胸腺指数和血清溶血素水平,增强免疫低下小鼠的DTH。结论肝康乐煎剂可以增强免疫低下小鼠的免疫功能。     

糖尿病患者怎样防治肺部感染？

部感染是糖尿病患者常见的急性并发症之一。糖尿病患者易合并感染的主要原因有：第一，高血糖引发的机体免疫功能低下。在高糖环境下，白细胞趋化性下降，吞噬作用减弱，杀伤力降低，致使糖尿病患者防御功能减弱；第二，高血糖促进细菌超常分化繁殖；第三，患者常伴有各种慢性并发症包括血管和神经系统病变，     

十全大补汤在抗真菌治疗中的辅助作用实验研究

通过实验性动物白念珠菌全身感染，研究在免疫功能低下状态，抗真菌经单纯治疗和与中药方剂十全大补汤伍用，其疗效的差异。实验结果证明：十全大补汤无直接抗真菌活性；抗真菌药对处于免疫功能低下状态的动物，其疗效也不十分理想。抗真菌药在治疗全身白念珠菌感染时，如用十全大补汤，通过后者ＢＲＭ样作用，可改善机体免疫状态，从而提高抗真菌药的疗效，与单纯使用抗真菌治疗有明显差异（Ｐ＜０．０５）。据此可以认为：处于免疫功能低下的机体，一旦感染真菌，在抗真菌治疗同时伍用十全大补汤有利于提高抗真菌药物的疗效。     

抗乙肝免疫核糖核酸治疗慢性乙肝100例

抗乙肝免疫核糖核酸(IRNA)是从用乙肝抗原免疫羊的淋巴结、脾脏和肝脏中提取的核糖核酸,是一种免疫调节剂,可提高机体细胞免疫功能,诱导产生干扰素。用于治疗乙肝,可使乙肝抗原阴转,抗体产生,肝功能恢复正常。 一般资料:治疗组100例均符合1984年病毒性肝炎学术会议修订的诊断分型标准,     

脾虚证进程中小鼠特异性/非特异性免疫功能变化及中药的干预作用

目的 观察脾虚证进程中小鼠特异性/非特异性免疫功能的变化及中药敦煌大宝胶囊对其免疫功能的影响.方法 受试动物随机分为空白对照组、模型组、敦煌大宝胶囊大、中、小治疗组,阳性对照组,每组8只.建立脾虚证小鼠模型,中药干预后观测各组小鼠腹腔巨噬细胞吞噬率和吞噬指数;ConA,LPS诱导的T、B淋巴细胞增殖反应及NK细胞活性等指标.结果 脾虚证进程中小鼠特异性/非特异性免疫功能低下(P＜0.05).经中药干预后,与模型组比较,敦煌大宝胶囊治疗组小鼠腹腔巨噬细胞吞噬率和吞噬指数;ConA,LPS诱导的T、B淋巴细胞增殖反应及NK细胞活性显著升高,差异具有统计学意义(P<0.05).结论 脾虚证进程中小鼠特异性/非特异性免疫功能低下,敦煌大宝胶囊对脾虚证小鼠免疫功能紊乱具有明显改善作用.     

乙肝多肽疫苗和转移因子对无症状HBsAg携带者淋巴细胞转化的影响

无症状HBsAg携带者的免疫功能异常表现在对HBsAg的无反应性和细胞免疫功能低下。作者等观察了用乙肝多肽疫苗和正常人脾转移因子联合治疗后,无症状HBsAg携带者的淋巴细胞转化功能的变化和对HBsAg携带状态的影响。报告于下。     

有机锗调节老年人免疫功能的研究（附60例慢性支气管炎病人临床观察）

慢性支气管炎是老年人的常见病、多发病，病人的免疫功能均有不同程度的下降。本组观察对象90例，研究有机锗对老年人免疫功能的调节作用，现报告如下：     

隐隐子虫动物模型的建立

本文通过饮水给予免疫抑制药和用人源隐孢子虫卵囊感染ＮＩＨ小鼠，建立了隐孢子虫感染小鼠模型。实验结果显示：免疫功能抑制组比正常组易感，两者感染度有显著性差异。通过动物实验进一步证明免疫功能正常宿主感染隐孢子虫为自限性感染，免疫功能低下或缺陷者感染隐孢子虫可引起严重腹泻甚至死亡.     

Vitamin D deficiency modulates Graves' hyperthyroidism induced in BALB/c mice by thyrotropin receptor immunization

TSH receptor (TSHR) antibodies and hyperthyroidism are induced by immunizing mice with adenovirus encoding the TSHR or its A-subunit. Depleting regulatory T cells (Treg) exacerbates thyrotoxicosis in susceptible BALB/c mice and induces hyperthyroidism in normally resistant C57BL/6 mice. Vitamin D plays an important role in immunity; high dietary vitamin D intake suppresses (and low intake enhances) adaptive immune responses. Vitamin D-induced immunosuppression may enhance Treg. Therefore, we hypothesized that decreased vitamin D intake would mimic Treg depletion and enhance hyperthyroidism induced by A-subunit adenovirus immunization. BALB/c mice had a reduced ability vs. C57BL/6 mice to generate the active metabolite of vitamin D (1,25-dihydroxyvitamin D3). Vitamin D deficiency induced subtle immune changes in BALB/c (not C57BL/6) mice. Compared with mice fed regular chow, vitamin D-deprived BALB/c mice had fewer splenic B cells and decreased interferon-gamma responses to mitogen and lacked memory T-cell responses to A-subunit protein. However, vitamin D deficiency did not alter TSHR antibody responses measured by ELISA, TSH binding inhibition, or cAMP generation from TSHR-expressing cells. Unexpectedly, compared with vitamin D-sufficient mice, vitamin D-deficient BALB/c mice had lower preimmunization T(4) levels and developed persistent hyperthyroidism. This difference was unrelated to the immunological changes between vitamin D-deficient or -sufficient animals. Previously, we found that different chromosomes or loci confer susceptibility to TSHR antibody induction vs. thyroid function. Our present studies provide evidence that an environmental factor, vitamin D, has only minor effects on induced immunity to the TSHR but directly affects thyroid function in mice.     

Immunoregulation of genetically controlled acquired responses to Leishmania donovani infection in mice: the effects of parasite dose, cyclophosphamide and sublethal irradiation

On a B10 (Lshs) genetic background, the development of acquired T cell mediated immunity to Leishmania donovani infection in mice is under H-2 linked genetic control. Following intravenous inoculation of 10(7) amastigotes three phenotypic patterns of recovery have been described: 'early cure' (H-2r,s), 'cure' (H-2b) and 'non-cure' (H-2d,q,f). In an attempt to determine the immunological basis for this H-2 linked genetic control the effects of varying parasite dose (5 x 10(3) to 5 x 10(7) amastigotes) and of pre-treatments with cyclophosphamide (50 or 200 mg/kg body weight CY) or sublethal irradiation (100 or 550 rad) on the course of infection, and on circulating anti-leishmanial IgG levels, were examined in strains representative of the three phenotypes: B10.D2/n (H-2d), C57BL/10ScSn (H-2b) and B10.RIII (H-2r). It was found that with low parasite doses (5 x 10(3) or 5 x 10(4)) 'non-cure' mice presented a 'cure' profile whilst raising the dose (5 x 10(7)) caused some perturbation of the normal self-curing response in 'cure' (but not 'early cure') mice. The highest dose did not, however, lead to progressive disease in the genetically non-cure strain. For the parasite dose experiments circulating anti-leishmanial IgG levels were higher in the early cure and cure strains than in the H-2d non-cure strain. The higher doses of CY and sublethal irradiation administered prior to infection had a clear prophylactic effect on the non-cure strain with some effect also observed in cure and early cure strains. This was thought to be due to deletion of the precursors of T suppressor (TS) cells suppressing cell-mediated immunity. Resolution of the liver parasite load in pre-treated mice took place despite minimal or undetectable levels of circulating anti-leishmanial IgG. Similarly, the earlier resolution of parasite load in pre-treated cure and early cure mice occurred even though the antibody response was severely reduced. This suggests that the high antibody responses observed in early cure and cure strains do not normally mediate cure and may simply reflect the independent effect of H-2 on T helper function or the humoral response.     

Photodynamic therapy plus low-dose cyclophosphamide generates antitumor immunity in a mouse model

Photodynamic therapy (PDT) is a modality for the treatment of cancer involving excitation of nontoxic photosensitizers with harmless visible light-producing cytotoxic reactive oxygen species. PDT causes apoptosis and necrosis of tumor cells, destruction of the tumor blood supply, and activation of the immune system. The objective of this study was to compare in an animal model of metastatic cancer PDT alone and PDT combined with low-dose cyclophosphamide (CY) a treatment that has been proposed to deplete regulatory T cells (T-regs) and increase the immune response to some tumors. We used J774 tumors (a highly metastatic reticulum cell sarcoma line) and PDT with benzoporphyrin derivative monoacid ring A, verteporfin for injection (BPD; 1-mg/kg injected i.v. followed after 15 min by 150 J/cm(2) of 690-nm light). CY (50 or 150 mg/kg i.p.) was injected 48 h before light delivery. PDT alone led to tumor regressions and a survival advantage but no permanent cures were obtained. BPD-PDT in combination with low-dose CY (but not high-dose CY) led to 70% permanent cures. Low-dose CY alone gave no permanent cures but did provide a survival advantage and was shown to reduce CD4+FoxP3+ T-regs in lymph nodes, whereas high-dose CY reduced other lymphocyte classes as well. Cured animals were rechallenged with J774 cells, and the tumors were rejected in 71% of mice. Cured mice had tumor-specific T cells in spleens as determined by a (51)Cr release assay. We conclude that low-dose CY depletes T-regs and potentiates BPD-PDT, leading to tumor cures and memory immunity.     

复方柴郁汤对小鼠免疫性肝损伤的影响

目的：观察中药复方柴郁汤对小鼠免疫性肝损伤的影响。方法：将72只小鼠随机分为空白组、病理组、日达仙组以及复方柴郁汤大、中、小剂量组，采用BCG＋LPS造模，观察并比较各组小鼠血清ALT、AST含量以及肝脏病理结构。结果：各治疗组和日达仙组的ALT、AST值明显低于病理组（P〈0．01），组织结构明显优于病理组（P〈0.01）。其中中剂量组又优于其他治疗组和对照组（P〈0．05）。结论：复方柴郁汤能明显降低免疫性肝损伤小鼠血清ALT、AST的活力单位．减轻其免疫性肝损伤程度。     

加味左金丸对大鼠胃癌前病变增殖细胞核抗原及B淋巴细胞瘤/白血病-2蛋白表达的影响

[目的] 观察加味左金丸对大鼠萎缩性胃炎(CAG)癌前病变增殖细胞核抗原(PCNA)及B淋巴细胞瘤/白血病-2(Bcl- 2)蛋白表达的影响,并探讨其治疗CAG癌前病变的可能机制。[方法] 采用SP法检测大鼠胃癌前病变自然恢复组,加味左金丸高、中、低剂量组,维甲酸组和正常组大鼠胃黏膜组织中PCNA、Bcl -2 蛋白表达的情况,并计算细胞增殖指数(PI)。[结果] 各治疗组PI及Bcl- 2 蛋白阳性率与自然恢复组比较差异有统计学意义(P<0 .01或<0 .05);其中加味左金丸各治疗组PI值与维甲酸组比较差异有统计学意义(P<0 .05)。[结论] 加味左金丸可能通过对抗PCNA、Bcl 2的激活而抑制PCNA、Bcl -2蛋白的表达发挥治疗作用。     

Beta-glucosylceramide: a novel method for enhancement of natural killer T lymphoycte plasticity in murine models of immune-mediated disorders

BACKGROUND: beta-Glucosylceramide, a naturally occurring glycolipid, exerts modulatory effects on natural killer T (NKT) lymphocytes. AIM: To determine whether beta-glucosylceramide can alter NKT function in opposite directions, colitis was induced by intracolonic installation of trinitrobenzenesulphonic acid, and hepatocellular carcinoma (HCC) was induced by transplantation of Hep3B cells. METHODS: The immunological effect of beta-glucosylceramide was assessed by analysis of intrahepatic and intrasplenic lymphocyte populations, serum cytokines and STAT protein expression. RESULTS: Administration of beta-glucosylceramide led to alleviation of colitis and to suppression of HCC, manifested by improved survival and decreased tumour volume. The beneficial effects were associated with an opposite immunological effect in the two models: the peripheral:intrahepatic CD4:CD8 lymphocyte ratio increased in the colitis model and decreased in the HCC group. The peripheral:intrahepatic NKT lymphocyte ratio decreased in beta-glucosylceramide-treated mice solely in the HCC model. The effect of beta-glucosylceramide was associated with decreased STAT1 and 4 expression, and with overexpression of STAT6, along with decreased interferon gamma levels in the colitis model, whereas an opposite effect was noted in the HCC model. CONCLUSIONS: beta-glucosylceramide alleviates immunologically incongruous disorders and may be associated with "fine tuning" of immune responses, by changes in plasticity of NKT lymphocytes.     

温胃舒冲剂对小鼠慢性萎缩性胃炎的保护作用及其机理初探

温胃舒冲剂是根据临床实践组成的中药复方制剂．为了探讨其作用机理．用小鼠造成３种模型：去氧胆酸钠（ＤＯＣＡ）造成慢性萎缩性胃炎（ＣＡＧ）模型；ＤＯＣＡ＋甲疏基咪唑造成 ＣＡＧ－阳虚模型，ＤＯＣＡ＋甲状腺＋利血平造成 ＣＡＧ－阴虚模型。以血浆中环磷酸腺苷（ｃＡＭＰ ）、环磷酸鸟苷（ｃＧＭＰ）观察其治疗作用。结果表明，温胃舒能降低ＣＡＧ模型小鼠的ｃＡＭＰ、ｃＧＭＰ．也能降低ＣＡＧ－阳虚模型小鼠的ｃＧＭＰ，与模型对照组比较均Ｐ＜０．０５～０．０１。此外．结果还表明温胃舒冲剂有镇痛、抗炎和抑制胃肠推进运动、并能提高大鼠淋巴细胞转化率、血清ＩｇＧ水平。     

CXCL16 participates in pathogenesis of immunological liver injury by regulating T lymphocyte infiltration in liver tissue

AIM: To investigate the role of CXCL16 in the pathogenesis of immunological liver injury and to explore the possible mechanism of T lymphocyte infiltration regulated by CXCL16. METHODS: Immunological liver injury in murine model was induced by Bacille Calmette-Guerin and lipopolysaccharide. Expression pattern and distribution of CXCL16 were examined by real-time quantitative RT-PCR and immunohistochemical analysis. Anti-CXCL16 antibody was administrated in vivo to investigate its effect on T-cell recruitment and acute hepatic necrosis. The survival of murine model was also evaluated. RESULTS: The murine immunological liver injury model was successfully established. CXCL16 expression increased and predominantly distributed in periportal areas and vascular endothelia in injured liver tissues. Administration of anti-CXCL16 Ab protected the mice from death and acute liver damage. Approximately 70% of the mice survived for 72 h in the anti-CXCL16 Ab treatment group, whereas 80% died within 72 h in control Ab group. The number of liver-infiltrating T lymphocytes was significantly reduced from 1.01×107 to 3.52×106/liver, compared with control Ab treatment. CONCLUSION: CXCL16 is involved in immunological liver injury by regulating T lymphocyte infiltration in liver tissue.     

芪黄冲剂对慢性乙型肝炎患者免疫功能的影响

目的：观察芪黄冲剂对慢性乙型病毒性肝炎免疫功能的影响。方法：治疗组以芪黄冲剂治疗,对照组以乙肝清热解毒冲剂合乙肝养阴活血冲剂治疗。两组患者采用间接免疫荧光法检测,治疗前后免疫球蛋白ＩｇＧ、ＩｇＭ、ＩｇＡ、Ｔ淋巴细胞亚群ＣＤ３＾＋、ＣＤ４＾＋、ＣＤ８＾＋、ＣＤ４＾＋／ＣＤ８＾＋、ＩＬ－２、ＩＬ－６、ＴＮＦ、ＮＫ。结果：芪黄冲剂具有益气活血,滋养肝肾兼以清热解毒作用,能升高ＣＤ４＾＋、ＮＫ细胞,提高ＣＤ４＾＋／ＣＤ８＾＋比值及ＩＬ－２水平,降低ＣＥ８＾＋,尤其对ＣＤ４＾＋、ＣＤ４＾＋／ＣＤ８＾＋、ＮＫ细胞以及ＩＬ０２的调整作用优于对照组（Ｐ〈０．０５￣０．０１）,能显著降低ＩＬ－６及ＴＮＦ水平（Ｐ〈０．０５￣０．０１）。同时还能降低ＩｇＧ、ＩｇＭ、ＩｇＳ,其中对ＩｇＡ的降低作用显著优于对照组。结论：芪黄冲剂不仅具有     

Aerogenic vaccination of mice with Mycobacterium bovis BCG

The course of infection with Mycobacterium bovis BCG Pasteur was followed against time in groups of mice vaccinated by either the aerogenic or subcutaneous route. The generation of acquired protective immunity and immunological memory was determined in each group by adoptive immunisation procedures. In addition, subcutaneously vaccinated mice were tested for their ability to resist an aerogenic challenge with a lethal dose of M. tuberculosis. No overall qualitative differences in the magnitude or longevity of antituberculosis immunity in mice vaccinated by the two procedures were observed. It is concluded that aerogenic vaccination offers no immunological advantage over vaccination by the subcutaneous route.