苦瓜皂甙对衰老小鼠免疫功能的影响

目的 :　探讨苦瓜皂甙对衰老小鼠免疫功能的影响。方法 :　 1 5 mo雌性昆明小鼠 ,随机分为老年对照组 ( SC)、实验 组 ( E1 )、实验 2组 ( E2 ) ,SC饮用自来水、E1、E2两组分别饮含有1 0 0 mg/L和 2 0 0 mg/L的苦瓜皂甙水。饲养 5 w后 ,处死动物 ,取标本待测。同时制备衰老小鼠脾细胞、腹腔巨噬细胞、胸腺细胞 ,分别加入不同浓度的苦瓜皂甙 ( 2 5 mg/L和 5 0 mg/L) ,培养后待测。结果 :　苦瓜皂甙不影响脾脏指数 ,但胸腺指数有升高趋势 ,实验组吞噬指数、血清 IL- 2水平明显升高 ,且 E2高于 E1 ( P<0 .0 5 )。苦瓜皂甙能明显增加胸腺中 CD8+ - T细胞数 ,显著降低胸腺和脾脏中 CD+ CD8+ 双阳性 T细胞数。体外实验表明 ,苦瓜皂甙不但可促进脾脏分泌 IL - 2 ,还可显著增强腹腔巨噬细胞分泌 TNFα,但不影响胸腺细胞凋亡百分率。结论 :　苦瓜皂甙可通过改变 T细胞各亚群比例 ,促进 IL- 2分泌 ,增强吞噬指数 ,提高衰老小鼠免疫功能。     

醋酸舍莫瑞林的免疫活性研究

目的　观察醋酸舍莫瑞林对免疫抑制模型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 ,建立免疫功能低下模型 ,腹腔注射醋酸舍莫瑞林进行体内拮抗实验。测定胸腺指数、脾脏指数、巨噬细胞吞噬功能、T淋巴细胞的增殖指数、耳肿胀度、血清IL - 2的含量。结果　醋酸舍莫瑞林 ( 0 18,0 36mg/kg)能显著提高被环磷酰胺抑制的胸腺和脾脏重量 (P <0 0 1) ;使巨噬细胞吞噬功能明显增加 ,并能拮抗环磷酰胺对小鼠脾脏T淋巴细胞增殖、二硝基氯苯 (DNCB)诱导的迟发型超敏反应和IL - 2产生的免疫抑制作用。结论　醋酸舍莫瑞林能拮抗环磷酰胺所引发的免疫抑制作用     

黑加仑多糖对免疫功能调节作用的实验研究

目的:研究黑加仑多糖对免疫功能低下小鼠的免疫调节作用。方法:给小鼠腹腔注射环磷酰胺,建立小鼠免疫功能低下模型后,以0.4,0.8和1.6g/kg的黑加仑多糖灌胃,连续10d,另设模型对照组和正常对照组。观察免疫低下小鼠的脾、胸腺指数变化情况;用分光光度法测定小鼠巨噬细胞吞噬数、抗体分泌细胞生成数、血清溶血素和IL-2等免疫指标的含量。结果:黑加仑多糖高、中、低剂量组对免疫功能低下小鼠的脾、胸腺指数有增强作用,IL-2产生增加,增强血清溶血素的功能(P0.05),其中高、中剂量组对巨噬细胞吞噬功能有增强作用(P0.05)。黑加仑多糖高剂量组对免疫功能低下小鼠抗体分泌细胞功能有增强作用(P0.05)。结论:黑加仑多糖具有增强免疫功能的作用。     

脂多糖体外刺激对小鼠B10细胞的影响

目的:探索脂多糖(LPS)体外刺激对小鼠B10细胞的影响。方法:在LPS刺激下,体外培养小鼠脾脏和腹腔细胞5h或48h,流式细胞仪分析CD19+IL-10+B细胞比例。结果:PIM刺激5h,小鼠脾脏和腹腔CD19+IL-10+B细胞比例分别升高至1.22%和14.82%(P<0.01),在PIM刺激的基础上加入LPS,小鼠脾脏和腹腔中CD19+IL-10+B细胞比例分别升高至平均2.35%和26.58%(P<0.01)。LPS刺激48h可进一步升高CD19+IL-10+B细胞比例,脾脏和腹腔分别为6.42%和38.38%,明显高于PIM48h刺激组(P<0.01)和L+PIM5h刺激组(P<0.05),但LPS刺激48h不改变CD5、CD1d的表达水平。结论:体外刺激5h时,L+PIM刺激可促进小鼠B10细胞活化;刺激48h时,LPS可进一步促进B10细胞IL-10的表达,这一作用可能是通过诱导B10前体细胞成熟实现的。     

番茄、胡萝卜混合汁乳酸菌发酵液对小鼠免疫功能的影响

目的探讨番茄、胡萝卜混合汁乳酸菌发酵液对免疫力低下小鼠免疫功能的影响。方法以番茄、胡萝卜汁发酵液为受试物,以免疫力低下小鼠为研究对象。研究发酵液对小鼠的外周血白细胞数,脾、胸腺指数,巨噬细胞吞噬功能,脾脏T淋巴细胞转化功能,白介素2(IL-2)水平,白介素4(IL-4)水平,抗体分泌功能,血清溶血素(HC50)等免疫指标的影响。结果发酵液高、中剂量组的巨噬细胞吞噬功能(吸光度0.57±0.03,0.51±0.02)均明显高于模型组(0.46±0.03,P<0.05);高剂量组脾T淋巴细胞转化功能(吸光度0.032±0.003)明显强于模型组(0.027±0.003,P<0.05);高剂量组脾细胞抗体的分泌功能(吸光度0.26±0.01)也明显强于模型组(0.18±0.03,P<0.05)。高剂量组血清中IL-2含量〔(15.83±1.29)pg.mL-1〕明显多于模型组(9.62±1.36,P<0.05)。结论番茄、胡萝卜发酵液对免疫力低下小鼠免疫功能有一定的增强作用。     

紫贻贝粗多糖提取物对小鼠免疫相关因子的影响

目的研究紫贻贝多糖对免疫力低下小鼠的免疫相关因子的影响。方法 30只6～8周龄,体重20 g左右,雌雄随机的ICR小鼠,分成正常对照(Control)、环磷酰胺(CTX)处理的免疫抑制(CTX)、高、中、低不同剂量紫贻贝粗多糖提取物(H-MEP、M-MEP、L-MEP)5组,每组6只。H-MEP、M-MEP、L-MEP三组每天分别腹腔注射0.1 ml 16、8和2的紫贻贝粗多糖提取物1w后,与CTX组一起腹腔注射CTX,再注射相应浓度的紫贻贝粗多糖提取物5d后处死小鼠,测定小鼠脾脏NK细胞的杀伤力,小鼠腹腔巨噬细胞产生的NO量以及血清中IL-2、IL-4、IFN-γ、TNF-α的含量。结果 H-MEP、M-MEP、L-MEP组小鼠NK细胞的杀伤力显著强于CTX组(P﹤0.05),H-MEP、M-MEP组甚至超过正常对照组(P﹤0.05);H-MEP、M-MEP组小鼠腹腔巨噬细胞产生的NO量明显超过CTX组(P<0.01),H-MEP组还显著超过正常对照组;高、中剂量多糖提取物组小鼠血清中IL-2显著高于CTX组,而IL-4与CTX组和正常对照组无差异;M-MEP组小鼠中血清IFN-γ显著高于免疫抑制组,H-MEP组TNF-α的含量显著高于免疫抑制组(P﹤0.05),与正常对照组,也明显增强(P﹤0.05)。结论紫贻贝多糖能上调免疫抑制小鼠的Th1细胞功能,纠正CTX引起的免疫抑制状态下的Th1向Th2形成的漂移,增强细胞免疫功能。     

甲型肝炎灭活疫苗(L-8株)口服及腹腔注射Bal b/c小鼠的免疫反应评价

目的　比较评价甲型肝炎(甲肝)灭活疫苗(L 8株)不同途径接种Balb/c小鼠所诱导产生的免疫效应。方法将32 0EU/0 5ml的实验疫苗1次口服及腹腔注射免疫实验动物,于2周、4周时收集血液样本,用酶联免疫吸附试验(ELISA)方法检测抗体反应,同时动态检测免疫小鼠外周血T淋巴细胞亚群及肿瘤坏死因子(TNF) α、干扰素(IFN) γ。结果　不论是腹腔注射或是口服免疫均能诱导产生良好有效的体液免疫效应。腹腔免疫后CD+ 4 T细胞百分比轻微下降,而CD+ 8T细胞百分比上升趋势及幅度明显,CD+ 4 /CD+ 8比值明显下降;而口服免疫小鼠外周血CD+ 4 T细胞百分比持续上升,CD+ 8T细胞百分比亦同步升高,两者上升幅度基本一致,CD+ 4 /CD+ 8比值无明显改变。另外,两种途径免疫接种均可诱导产生高滴度的内源性IFN γ。结论　有必要对甲肝灭活疫苗口服免疫的机制及其开发利用作进一步的研究。     

白藜芦醇对脂多糖诱导小鼠腹腔巨噬细胞炎性因子生成的调控

目的探讨白藜芦醇(Res)对脂多糖(LPS)诱导小鼠腹腔巨噬细胞核因子-κB(NF-κB)活化及炎性细胞因子[肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)]基因表达的调节。方法分别用1mg/LLPS或25mmol/LRes+1mg/LLPS处理体外培养的小鼠巨噬细胞,采用电泳迁移率改变分析法(EMSA)检测细胞中NF-κB活性,逆转录-聚合酶链反应(RT-PCR)和酶联免疫吸附法(ELISA)检测细胞中TNF-α、IL-1β、IL-6mRNA和蛋白的表达。结果LPS组NF-κB活性和TNF-α、IL-1β、IL-6含量在刺激后6～12h明显高于正常对照组(P<0.001),而Res+LPS组NF-κB活性和TNF-α、IL-1β、IL-6含量均显著低于LPS组(P<0.005)。结论LPS可诱导巨噬细胞NF-κB活化,导致TNF-α、IL-1β、IL-6基因表达增强,而Res能抑制NF-κB活化而调节TNF-α、IL-1β、IL-6基因的表达。     

慢性紫外线暴露下丁羟甲苯对小鼠部分免疫功能的保护作用

目的　探讨抗氧化剂丁羟甲苯在紫外线慢性暴露下对小鼠免疫系统的保护作用。方法　用单克隆抗体免疫法、中性红比色法、MTT法检测郎格罕细胞、腹腔巨噬细胞吞噬功能及脾脏T细胞增殖功能。结果　无毛鼠耳部和背部皮肤在紫外线慢性暴露下 ,表皮组织中免疫递呈细胞———郎格罕细胞数显著减少 ,脾脏T细胞增殖功能明显下降 ,提示紫外线可抑制细胞免疫。饮食中加入丁羟甲苯 (BHT)可以减轻小鼠郎格罕细胞数的下降 ,差异有显著性 (P <0 0 1) ,表明丁羟甲苯能拮抗紫外线对郎格罕细胞的免疫毒性。但丁羟甲苯对腹腔巨噬细胞吞噬功能、脾脏T细胞作用不显著。结论　丁羟甲苯在紫外线慢性暴露条件下 ,具有拮抗紫外线诱导的细胞免疫抑制的作用     

灵芝孢子油对免疫低下小鼠免疫调节机制的初步研究

目的采用免疫功能低下小鼠模型探讨灵芝孢子油免疫调节作用机制。方法将昆明小鼠随机分成模型对照组、灵芝孢子油组、正常对照组,每组10只;模型对照组、灵芝孢子油组分别腹腔注射40mg.kg-1.-1)环磷酰胺建立免疫功能低下小鼠模型,正常对照组腹腔注射生理盐水(0.9%)0.1ml/10g BW;同时灵芝孢子油组150mg/kg,正常和模型对照组灌胃玉米油0.1ml/10g BW,灌胃1次/A,连续30d;用ELISA试剂盒检测小鼠血清TNF-α、IFN-$水平,半定量PCR检测小鼠脾脏、胸腺IL-2、IL-10、IL-12、IL-4、IFN-$、TNF-α基因表达量,初步探讨灵芝孢子油的免疫调节机制。结果灵芝孢子油明显提高环磷酰胺免疫低下模型小鼠血清中TNF-α、IFN-$的含量,脾脏和胸腺中IL-2、IL-10、IL-12、IL-4、TNF-α和IFN-$mRNA的表达量,与模型对照组间差异显著(P≤0.05)。结论灵芝孢子油通过增强细胞因子的分泌、表达进行免疫调节。     

Effects of elm bark (Ulmus davidiana var. japonica) extracts on the modulation of immunocompetence in mice

The immunomodulative effects of elm bark extract were studied in vitro by the proliferation of splenocytes and the production capacity of three kinds of cytokines [interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha] by mouse peritoneal macrophages cultured with various fractions (methanol, hexane, chloroform, ethyl acetate, butanol, and water) of elm bark extract. Splenocyte proliferation and cell viability of peritoneal macrophages were increased with concentrations of polar fractions, such as butanol and water, in the range of 1-500 microg/mL. Significantly higher levels of the production of all three cytokines were detected with supplementation of methanol extract compared with other fractions. In order to elucidate its effect in vivo, elm bark water extract was orally administrated every other day for 2 weeks. Proliferation of splenocytes and the production capacity of cytokines (IL-1beta, IL-6, and TNF-alpha) by mouse peritoneal macrophages were used as indices for immune activity. Splenocyte proliferation induced by elm bark with lipopolysaccharide or concanavalin A stimulation was enhanced at 500 mg/kg of body weight concentrations compared to that of the control group. In the case of cytokines, the highest production of IL-6 and TNF was detected at 500 mg/kg of body weight concentrations. In conclusion, this study suggests through in vitro and in vivo experiments that Ulmus davidiana var. japonica (elm bark) extracts may enhance the immunocompetent properties such as splenocyte proliferation and cytokine production capacity by activated macrophages and have a protective effect in mice.     

Antigen-driven murine CD4+ T lymphocyte proliferation and interleukin-2 production are diminished by dietary (n-3) polyunsaturated fatty acids

This study is the first to describe the impact of consuming a diet rich in (n-3) polyunsaturated fatty acids (PUFA) from fish oil on antigen-driven activation of naive CD4+ T lymphocytes. To accomplish this, we used lymphocytes isolated from T cell receptor (TCR) transgenic mice (i.e., DO11.10). A large portion of the T lymphocytes from these mice expresses a TCR specific for a peptide within the ovalbumin (OVA) molecule (OVA(323-339)). When this antigen is presented in the context of major histocompatibility complex I-A(d) with costimulation, these naive CD4+ T cells become activated, produce interleukin (IL)-2 and clonally expand. (n-3) PUFA enrichment was accomplished by feeding DO11.10 mice one of two nutritionally complete experimental diets that differed only in the source of fat: lard or menhaden fish oil [high in (n-3) PUFA]. After 2 wk of consuming the experimental diets, lymphocytes were isolated from the spleen of each mouse, then cultured in the presence of antigen (i.e., OVA(323-339)) or concanavalin A (Con A), a nonspecific, polyclonal T cell stimulus. IL-2 production and lymphocyte proliferation were determined after 48 and 72 h, respectively. Naive CD4+ T lymphocytes from fish oil-fed mice stimulated with antigen produced less IL-2 ( approximately 33%; P < 0.001) and proliferated to a lesser extent ( approximately 50%; P < 0.0001) than the same cells from lard-fed DO11.10 mice. When stimulated with Con A, (n-3) PUFA did not affect either proliferation or IL-2 production. In summary, we report for the first time that feeding mice a diet enriched with (n-3) PUFA reduces in vitro antigen-stimulated production of IL-2 and subsequent proliferation of naive CD4+ T lymphocytes.     

不同剂量隐孢子虫感染正常和免疫抑制小鼠的效应研究

目的探讨昆明小鼠在灌服地塞米松、地塞米松+隐孢子虫卵囊(150万)、地塞米松+隐孢子虫卵囊(300万)的免疫功能的变化。方法采用MTT法检测40只昆明小鼠的免疫功能。随机分组:空白对照组(n=10),免疫抑制组(n=10),免疫抑制+隐孢子虫卵囊150万(n=10),免疫抑制+隐孢子虫卵囊300万(n=10)。结果实验组小鼠与对照组小鼠比较,巨噬细胞吞噬功能明显降低,T、B淋巴细胞的增殖明显降低,NK细胞活性均明显降低(p<0.01)。结论40只昆明小鼠吞噬功能、脾细胞增殖、NK细胞活性检测结果见表(1-3),从表中可以看出,实验组小鼠与对照组小鼠三项检测指标比较均有明显降低,差异显著(P<0.01),实验组小鼠各组间比较,差异无显著性(P>0.05)。     

Immunization with adenovirus LIGHT-engineered dendritic cells induces potent T cell responses and therapeutic immunity in HBV transgenic mice

LIGHT, a TNF superfamily member (TNFSF14), is a type II transmembrane protein expressed on activated T cells and immature dendritic cells (DCs). However, the expression of LIGHT on mature DCs is down-regulated. Recent studies demonstrated that LIGHT provides potent costimulatory activity for T cells, enhancing proliferation and the production of Th1 cytokines independently of the B7-CD28 pathway. Here, we evaluated the effectiveness of peptide-pulsed DC-mediated antiviral immunity in HBV transgenic mice and the immunoadjuvant effect of LIGHT. The bone marrow-derived DCs were modified in vitro with an adenovirus (Ad) vector expressing mouse LIGHT (Ad-LIGHT), the expression of costimulatory molecules was up-regulated and the secretion of cytokines IL-12 and IFN-γ increased. LIGHT-modified DCs enhanced allostimulation for T cells in mixed lymphocyte reaction (MLR). HBV peptide-pulsed DCs elicited HBV specific CD8+ T cell response and reduced the level of HBsAg and HBV DNA in sera of HBV transgenic mice. Importantly, LIGHT-modified DCs could induce stronger antiviral immunity. These results support the concept that genetic modification of DCs with a recombinant LIGHT adenovirus vector may be a useful strategy for antiviral immunotherapy.     

Effect of a cocoa flavonoid-enriched diet on experimental autoimmune arthritis

Previously we established that a cocoa-enriched diet in young rats reduces specific antibody production and the T helper (Th) lymphocyte proportion in lymphoid tissues. The aim of the present study was to ascertain the modulatory ability of a cocoa flavonoid-enriched diet on collagen-induced arthritis (CIA), which is mediated by anti-collagen autoantibody response and Th lymphocyte activation. Female Louvain (LOU) rats were fed with a cocoa-enriched diet, beginning 2 weeks before CIA induction. Hind-paw swelling and serum cytokine and anti-collagen antibody concentrations were determined. Anti-collagen antibody-secreting cell counts and lymphocyte subset proportions were established in inguinal lymph nodes (ILN). Reactive oxygen species (ROS), nitric oxide (NO) and TNFα produced by peritoneal macrophages were determined. Although arthritic cocoa-fed rats showed a similar hind-paw swelling time course as the arthritic animals fed a standard diet, the cocoa intake was able to decrease specific IgG2a, IgG2b and IgG2c titres. Moreover, cocoa intake in CIA rats reduced ROS production, TNFα and NO release from peritoneal macrophages, and decreased the Th:cytotoxic T cell ratio in ILN. In conclusion, a cocoa flavonoid-enriched diet in LOU rats with CIA produced no effect on hind-paw swelling but was able to modulate the specific antibody response and also the Th lymphocyte proportion, as well as the synthesis of pro-inflammatory mediators from peritoneal macrophages. Therefore, a cocoa-enriched diet could be a good adjuvant therapy in disorders with oxidative stress or autoimmune pathogenesis.     

Increasing the dietary (n-3) to (n-6) polyunsaturated fatty acid ratio increases tumor necrosis factor production by murine resident peritoneal macrophages without an effect on elicited peritoneal macrophages.

Tumor necrosis factor (TNF), prostaglandin (PG) E2 and 6-keto-PGF1 alpha production by murine peritoneal macrophages was monitored following in vitro stimulation with lipopolysaccharide. Macrophages were obtained from mice fed diets containing increasing ratios of (n-3) to (n-6) fatty acids by addition of (n-3) polyunsaturated fatty acids (PUFA) to the (n-6) fatty acids in the diet, or by substituting (n-3) PUFA for the (n-6) fatty acids in the diet. Increasing the dietary (n-3) to (n-6) fatty acid ratio from 0 to 1 increased both cell-associated and secreted TNF production by resident peritoneal macrophages but did not affect TNF production by macrophages elicited with Complete Freund's Adjuvant (CFA). With increasing dietary (n-3): (n-6) ratio there was a decrease in the prostaglandin production by resident peritoneal macrophages, which may partly explain the increased TNF production. The CFA-elicited macrophages produced less prostaglandin than the resident macrophages, and the lower prostaglandin production may partly explain the lack of effect of dietary (n-3) PUFA on TNF production by CFA-elicited macrophages. Increasing the TNF production by resident macrophages with dietary (n-3) PUFA may be beneficial in enhancing antitumor actions and antipathogenicity; by not increasing the high TNF production of inflammatory macrophages, (n-3) PUFA may protect against undesirable systemic inflammatory effects of overproduction.     

Dietary fish oil increases tumor necrosis factor secretion but decreases interleukin-10 secretion by murine peritoneal macrophages

Dietary fish oil has immunomodulatory effects that are mediated in part by its effects on cytokines. Secretion of the inflammatory and the anti-inflammatory cytokines tumor necrosis factor (TNF) and interleukin (IL)-10 by murine resident peritoneal macrophages was monitored after ex vivo stimulation with lipopolysaccharide. Macrophages were obtained from mice fed a corn oil diet containing 200 g/kg corn oil or a fish oil diet containing 180 g/kg fish oil and 20 g/kg corn oil. Dietary fish oil increased secretion of the proinflammatory cytokine, TNF, but decreased secretion of the anti-inflammatory cytokine, IL-10. The cytokines appeared in the medium after 1.5 h and peaked at 6-12 h. Neutralizing antibodies against TNF and IL-10 had little effect on secretion of the other cytokine, indicating that the effects of fish oil on TNF and IL-10 secretion by these cells are independent of one another. Furthermore, although inhibiting prostaglandin production enhanced TNF secretion by macrophages from mice fed the corn oil diet, it did not affect IL-10 secretion by macrophages in this group. Blocking leukotriene B(4) production also did not affect IL-10 secretion in macrophages from mice fed a nonpurified diet. These results demonstrate that fish oil has an overall pro-inflammatory effect given its effects on secretion of both inflammatory and anti-inflammatory cytokines by resident peritoneal macrophages.     

Wool and grain dusts stimulate TNF secretion by alveolar macrophages in vitro.

OBJECTIVE: The aim of the study was to investigate the ability of two organic dusts, wool and grain, and their soluble leachates to stimulate secretion of tumour necrosis factor (TNF) by rat alveolar macrophages with special reference to the role of lipopolysaccharide (LPS). METHODS: Rat alveolar macrophages were isolated by bronchoalveolar lavage (BAL) and treated in vitro with whole dust, dust leachates, and a standard LPS preparation. TNF production was measured in supernatants with the L929 cell line bioassay. RESULTS: Both wool and grain dust samples were capable of stimulating TNF release from rat alveolar macrophages in a dose-dependent manner. The standard LPS preparation caused a dose-dependent secretion of TNF. Leachates prepared from the dusts contained LPS and also caused TNF release but leachable LPS could not account for the TNF release and it was clear that non-LPS leachable activity was present in the grain dust and that wool dust particles themselves were capable of causing release of TNF. The role of LPS in wool dust leachates was further investigated by treating peritoneal macrophages from two strains of mice, LPS responders (C3H) and LPS non-responders (C3H/HEJ), with LPS. The non-responder mouse macrophages produced very low concentrations of TNF in response to the wool dust leachates compared with the responders. CONCLUSIONS: LPS and other unidentified leachable substances present on the surface of grain dust, and to a lesser extent on wool dust, are a trigger for TNF release by lung macrophages. Wool dust particles themselves stimulate TNF. TNF release from macrophages could contribute to enhancement of inflammatory responses and symptoms of bronchitis and breathlessness in workers exposed to organic dusts such as wool and grain.     

Non PC liposome entrapped promastigote antigens elicit parasite specific CD8+ and CD4+ T-cell immune response and protect hamsters against visceral leishmaniasis

Leishmania donovani promastigote soluble antigens (sLAg) were encapsulated in non-phosphatidylcholine (non-PC) liposomes (escheriosomes) prepared from E. coli lipids. The escheriosome-based vaccine was investigated for its potential to elicit a protective immune response against experimental visceral leishmaniasis. The vaccine administration induced strong humoral as well as cell mediated immune responses both in hamsters and BALB/c mice. Immunization of BALB/c mice with escheriosome entrapped sLAg (EL-sLAg) elicited stronger CD8+ cytotoxic T lymphocyte (CTL) response as compared to sLAg entrapped in egg PC/chol liposome (EPC-sLAg) or sLAg administered with incomplete Freund's adjuvant (IFA-sLAg). EL-sLAg also induced the release of mixed (Th1 and Th2) types of cytokines in the immunized BALB/c mice. In addition, the delivery of sLAg via escheriosomes enhanced the expression of costimulatory signals (CD80 and CD86) as determined in peritoneal macrophages obtained from BALB/c mice. In another set of experiments, the EL-sLAg immunized hamsters were found to be better protected than those immunized with EPC-sLAg. The prophylaxis coincided with increased lymphocyte proliferation as well as high nitric oxide (NO) production by peritoneal macrophages among EL-sLAg immunized hamsters. Escheriosomes thus seem to have potential in delivering the antigen to cytosol of the antigen presenting cells (APCs) and in the development of liposome-based vaccine against leishmaniasis as well as other intracellular infections.