酵母培养物中葡多糖对机体免疫应答影响的研究

多糖被认为是一种广谱的非特异性免疫促进剂．能够增强人体的细胞免疫和体液免疫功能,可激活巨噬细胞,促进抗体的形成,激活补体及诱导产生干扰素等。利用多糖来提高养殖动物的免疫功能和机体防御能力,从而达到提高畜牧生产的目的,已经为越来越多的研究工作者所重视。酵母葡多糖是由葡葡糖组成的均一多糖。     

羊口疮病毒B2L基因DNA疫苗的构建及其诱导的免疫应答

为研究所构建羊口疮病毒(OrfV)B2L基因DNA疫苗诱导小鼠的免疫应答效果,本研究对pMD18T-B2L质粒进行PCR扩增,克隆B2L片段至pVAX1载体中构建pVAX1-B2L重组质粒,进行酶切和测序鉴定;采用脂质体法将pVAX1-B2L真核表达质粒转染MDBK细胞,RT-PCR和IFA法检测B2L基因在MDBK细胞中的转录和表达;将构建的DNA疫苗免疫KM系小鼠,采用间接ELISA、MTT和FACS法对其诱导的免疫应答进行研究。结果显示,成功构建pVAX1-B2L真核表达质粒,并在MDBK细胞中表达;免疫小鼠后,DNA疫苗能诱导小鼠产生OrfV特异性抗体;脾淋巴细胞增殖、CD4~+、CD8~+T淋巴细胞亚群百分比和IL-2、IFN-γ、IL-4细胞因子均高于pVAX1组和PBS组。结果表明,本研究制备的DNA疫苗能够诱导小鼠产生较高水平的体液免疫和细胞免疫应答。     

Vanadium stimulates immunological responses of chicks

In a continuation of studies on the interaction of dietary phosphorus (P) and vanadium (V) levels, studies have directed toward an examination of this interaction on the immune system of chicks. Antibody titers to sheep red blood cells (SRBC) were increased at 7 days post-inoculation (PI) by as little as 10 mg V/kg diet in the P-deficient group, while 50 mg V/kg was required in the P-supplemented group. At 14 days PI, only the 50 mg V/kg was significantly higher in both P-deficient and P-supplemented groups. At 21 days PI, vanadium had no significant effect. P-deficiency resulted in a decrease in the percentage of phagocytic macrophages obtained from the abdominal cavity and a decrease in the number of intracytoplasmic SRBC per phagocytic macrophage. These two criteria were increased by vanadium in both the P-deficient and P-supplemented animals. In P-supplemented animals, the CD4/CD8 ratios of lymphocytes obtained from the blood and spleen were increased by the inclusion of 50 mg V/kg diet. The IL-1-like activity of macrophage supernatants was not significantly affected by dietary V, but IL-6 activity was increased. Densitometric analysis of lysates of macrophages isolated from control and V-fed chicks for anti-protein-tyrosinephosphate (PTP) bands indicate that dietary V increased PTP. While the evidence is not clear that there is a P x V interaction in the immune system studies, it is clear that dietary V at the levels used results in a positive immune response of chicks, possibly mediated through increased PTP.     

New understanding of immunological mechanisms

The understanding and importance of antigen-specific immune responses after vaccination has completely changed in recent years. In the past, the focus for monitoring a vaccine-specific immune reaction was principally on the humoral branch of the immune system. The efficacy of vaccines, as assessed by the induction of protective immunity was mainly correlated with antibodies and antibody-titers. However, this correlation often failed and other parts of the immune system had also to be considered: namely, the innate immune system and the cellular branch of the antigen-specific immune system. With regard to vaccines, the innate immune system plays its main role in the effective activation of the antigen-specific immune response, in antigen-uptake and antigen-presentation. The dendritic cells (DCs) are the most important antigen presenting cells which present processed protein antigens (peptides) through MHC-molecules: MHC-class I, for the presentation of endogenous synthesised antigen; MHC-class II for exogenous antigen. Activation of DC leads to an enhanced production of cytokines and chemokines, to an up-regulation of co-stimulatory and activation molecules and also molecules for cell-cell interactions, e.g. interactions with cells of the antigen-specific immune system. T lymphocytes are the effector cells of the cellular branch of the antigen-specific immune system. They act either as MHC-class I-restricted cytolytic T lymphocytes (CTL) or as MHC-class II-restricted T-helper cells providing support for B lymphocytes (T(H)2) and the cellular part of the antigen-specific immune system (T(H)1). In order to achieve effective vaccination, the activation of all T-cell subpopulations is of advantage, but more important is the generation of antigen-specific memory T and B lymphocytes. In addition to these 'generic' immunological factors which are essential for the design of more efficacious vaccines, our detailed knowledge about feline and canine immune reactions after vaccination, which is still poor, has to be improved.     

Effects of road transportation on metabolic and immunological responses in Holstein heifers

This study examined the effects of road transportation on metabolic and immunological responses in dairy heifers. Twenty Holstein heifers in early pregnancy were divided into non‐transported (NT; n = 7) and transported (T; n = 13) groups. Blood was collected before transportation (BT), immediately after transportation for 100 km (T1) and 200 km (T2), and 24 h after transportation (AT). The T heifers had higher (P < 0.05) blood cortisol and non‐esterified fatty acid concentrations after T1 and T2 than did NT heifers. By contrast, the T heifers had lower (P < 0.05) serum triglyceride concentrations after T1 and T2 than had the NT heifers. The serum cortisol and triglyceride concentrations returned (P > 0.05) to the BT concentrations at 24 h AT in the T heifers. The granulocyte‐to‐lymphocyte ratio and the percentage of monocytes were higher (P < 0.05) after T2 in the T heifers than in the NT heifers, suggesting that transportation stress increased the numbers of innate immune cells. T heifers had higher (P < 0.01) plasma haptoglobin concentrations than NT heifers 24 h AT. In conclusion, transportation increased cortisol secretion and was correlated with increased metabolic responses and up‐regulation of peripheral innate immune cells in dairy heifers.     

Suppression of immunological responses in rabbits experimentally infected with bovine leukemia virus

Ten 2- to 4-month-old rabbits were inoculated subcutaneously with bovine leukemia virus (BLV)-infected bovine or sheep cells. By 6 weeks after inoculation all ten rabbits had converted to BLV antibody-positive, and BLV or BLV antigen was detected in lymphocytes from most of the rabbits tested, although there were few antigen-producing cells. Three rabbits showed continuous respiratory symptoms after infection and one died with pneumonia. Humoral immune responses against mouse serum were significantly suppressed in BLV-infected rabbits compared with non-infected control rabbits. The lymphocyte blastogenesis response was also suppressed in BLV-infected rabbits. At the time of necropsy, six rabbits showed pulmonary lesions; however, none of the BLV-infected rabbits had tumors during an observation period of over 1 year.     

Clinical and immunological responses of cats to feline herpesvirus type 1 infection

Cats which were challenged with feline herpesvirus type 1 developed clinical signs typical of feline viral rhinotracheitis whether or not they had been vaccinated against the disease. However, the clinical disease was less severe and of shorter duration in the vaccinated cats. After challenge, feline herpesvirus type 1 was recovered from the nostrils, oropharynx and peripheral blood leucocytes. Leucocytosis, primarily a neutrophilia, occurred initially in all the cats and was followed after clinical recovery by a mild lymphocytosis. Intradermal skin testing with feline herpesvirus type 1 and cell control antigens produced a positive delayed type skin reaction. Histology of the affected skin 72 hours after injection showed cellular infiltration, predominantly with eosinophils and neutrophils. The severity of the reaction was greater and more prolonged in the skin of the ear than in the skin of the abdomen.     

Ocular squamous cell carcinoma: immunological responses to tumour tissue and phytomitogens

Cows with histologically confirmed ocular squamous cell carcinoma were injected with autochthonous tumour brei in adjuvant. Lymphoproliferative responses of isolated peripheral blood lymphocytes exposed to phytomitogens and inhibition of cell migration indicated that afflicted animals were immunocompetent. Similar but lesser responses were evident when autochthonous tumour homogenates were used to stimulate lymphocytes.     

Antigen specific immunological responses of badgers (Meles meles) experimentally infected with Mycobacterium bovis

European badgers (Meles meles) are considered to be an important reservoir of infection for Mycobacterium bovis and are implicated in the transmission of tuberculosis to cattle in Ireland and Great Britain. Accurate tests are required for tuberculosis surveillance in badger populations and to provide a basis for the development of strategies, including vaccination, to reduce the incidence of the infection. In this study, we have developed an endobronchial M. bovis infection model in badgers in which we measured cell-mediated immune and serological responses for up to 24 weeks post-infection. Groups of badgers were subjected to necropsy at 6-week intervals and the gross lesion severity status compared with immune responses measured in blood samples taken throughout the course of the study. The panel of antigens included bovine and avian tuberculins (PPD) as well as single antigens, ESAT-6, CFP-10, MPB70, Rv3019c, Rv3873, Rv3878 and Rv3879, all known to be recognised by the immune system in other animal models of tuberculosis infection. Our results demonstrated that M. bovis infected badgers responded to specific antigens as early as 6 weeks post-infection, consistent with the presence of visible lesions. The data also revealed unique patterns of antigen recognition with high levels of PBMC proliferation in the presence of CFP-10 but low proliferation levels with ESAT-6. Using a multi-antigen print immunoassay (MAPIA), we were able to confirm that MPB83 is the dominant antigen recognised by serum antibodies in infected badgers.     

Epidemiological and immunological aspects of human crisis form factor in falciparum malaria: cell-mediated responses?

Crisis forms in malaria are degenerated intra-erythrocytic asexual parasites which appear at the time of immunologic crisis and thus may be part of the immune response to this disease. The factor(s) involved in this phenomenon are poorly understood, but are believed to be related to products of phagocyte activation. This hypothesis is supported by observations that animals, whose cell-mediated immune responses have been hyperstimulated by BCG, are protected from otherwise lethal malaria infections and their sera induce crisis forms in vitro. Many human serum samples collected from malaria-endemic areas of Sudan induce crisis forms in cultures of Plasmodium falciparum. Two popular models to explain this intra-erythrocytic, anti-parasitic action have been proposed: (i) the presence in the immune serum of a cytotoxic cytokine, crisis form factor, or (ii) that crisis forms result from oxidant stress generated during respiratory bursts associated with phagocyte activation, or indirectly by toxic products of lipid peroxidation produced by reactive oxygen species which appear in the serum during phagocyte respiratory bursts. Experimental evidence has been generated to support both of these hypotheses and both mechanisms may be involved in the induction of crisis forms.