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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several studies have addressed the question of the effects of starvation on immune function and changes in lymphocyte subsets. Patients with anorexia nervosa are severely malnourished, but there have been few studies of immune parameters in this group. For this reason, phenotypic markers of T cell function and activation were studied in 20 severely underweight patients with anorexia nervosa and again after a period of refeeding. The most significant finding was a reduction in the percentage and absolute number of CD8+ T cells in patients with anorexia, the result of a marked reduction in memory (CD45RO+RA-) CD8 cells. A tendency for recovery in numbers of this subset was seen after refeeding. A decreased memory:maive cell ratio was also seen among CD4 cells, but was less marked. Subtle abnormalities in activated CD4 and CD8 cells were also found in the patient group at the initial sampling, but did not follow any clear pattern. These findings indicate that starvation in anorexic patients is accompanied by a large change in memory CD8 T cells. It may be speculated that this relates to the perceived lack of symptomatic common viral infections in underweight anorexic patients and their return with the recovery of weight.
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PMID:T lymphocyte subpopulations in anorexia nervosa and refeeding. 932 79

The aim of this study was to characterise CD4+T-cells in equines, as these cells are pivotal in establishing immune responses or regulating established ones. Peripheral blood mononuclear cells from a pony immunised with ovalbumin were cultured in vitro in the presence of the specific antigen and autologous antigen presenting cells. During the antigen starvation phase, cells were maintained on recombinant equine IL-2. After 35 days of culture, most of the cells were CD4+, CD8-and sIg-. Cells proliferated specifically in the presence of antigen, as tested on day 42 of culture. These cells were analysed by in-situ hybridisation to detect m RNA for IL-2 and IL-4, the presence of which suggested the existence of of Th1- and Th2-like cells.
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PMID:Characterisation of equine T helper cells: demonstration of Th1- and Th2-like cells in long-term equine T-cell cultures. 1033 72

Thymic atrophy is a prominent feature of malnutrition. Forty-eight hours' starvation of normal mice reduced the total thymocyte count to 13% of that observed in freely fed controls, predominantly because of a diminution in the cortical CD4(+)CD8(+) thymocyte subpopulation. Prevention of the fasting-induced fall in the level of the adipocyte-derived hormone leptin by administering exogenous recombinant leptin protected mice from these starvation-induced thymic changes. The ob/ob mouse, which is unable to produce functional leptin because of a mutation in the obese gene, has impaired cellular immunity together with a marked reduction in the size and cellularity of the thymus. We found that ob/ob mice had a high level of thymocyte apoptosis resulting in a ratio of CD4(+)CD8(+) (cortical) to CD4(-)CD8(-) (precursor) thymocytes that was 4-fold lower than that observed in wild-type mice. Peripheral administration of recombinant leptin to ob/ob mice reduced thymocyte apoptosis and substantially increased both thymic cellularity and the CD4(+)CD8(+)/CD4(-)CD8(-) ratio. In contrast, a comparable weight loss in pair-fed PBS-treated ob/ob mice had no impact on thymocyte number. In vitro, leptin protected thymocytes from dexamethasone-induced apoptosis. These data indicate that reduced circulating leptin concentrations are pivotal in the pathogenesis of starvation-induced lymphoid atrophy.
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PMID:Leptin protects mice from starvation-induced lymphoid atrophy and increases thymic cellularity in ob/ob mice. 1052 43

Although the early identification of patients with suboptimal nutritional status can allow the implementation of nutritional intervention to enhance the ability of the body to fight infection and disease, currently no definitive test of nutritional status exists. Therefore, this study was conducted to identify possible functional indicators of acute nutritional deprivation. The effects of total nutritional deprivation and subsequent refeeding on lymphocyte functions and subpopulations were examined in 23 healthy cats. Peripheral blood samples were analyzed at various times during food deprivation and refeeding periods. During the food deprivation period, decreases were observed in leukocyte number (P: < 0.05), lymphocyte number (P: < 0.05), percentage of CD4(+) cells [before stimulation with concanavalin-A (Con-A); P: < 0.05] and the CD4/CD8 ratio (before stimulation with Con-A; P: < 0.01) compared with d 0. Increases were observed in the percentage of CD8(+) cells [before (P: < 0.05) and after (P: < 0.01) stimulation with Con-A] and in intracellular calcium (P: < 0.01) during acute starvation. During the refeeding period, increases were observed in the percentage of CD4(+) cells (before and after stimulation with Con-A; P: < 0.01), the percentage of CD8(+) cells (before stimulation with Con-A; P: < 0.05) and lymphocyte number (P: < 0.05) compared with d 7. Lymphocyte proliferative capacity tended to decrease (P: = 0.07) during starvation and increased (P: < 0.01) during the refeeding period. These findings suggest that a 7-d starvation period had immunosuppressive effects on cats and that these effects were not completely normalized during 7 d of refeeding. CD4(+)/CD8(+) subset alterations and CD4/CD8 ratio in conjunction with lymphocyte proliferation may be useful as indices of nutritional status.
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PMID:Acute starvation and subsequent refeeding affect lymphocyte subsets and proliferation in cats. 1101 70

The phenomenon of cell cannibalism, which generally refers to the engulfment of cells within other cells, was described in malignant tumors, but its biological significance is still largely unknown. In the present study, we investigated the occurrence, the in vivo relevance, and the underlying mechanisms of cannibalism in human melanoma. As first evidence, we observed that tumor cannibalism was clearly detectable in vivo in metastatic lesions of melanoma and often involved T cells, which could be found in a degraded state within tumor cells. Then, in vitro experiments confirmed that cannibalism of T cells was a property of metastatic melanoma cells but not of primary melanoma cells. In particular, morphologic analyses, including time-lapse cinematography and electron microscopy, revealed a sequence of events, in which metastatic melanoma cells were able to engulf and digest live autologous melanoma-specific CD8(+) T cells. Importantly, this cannibalistic activity significantly increased metastatic melanoma cell survival, particularly under starvation condition, supporting the evidence that tumor cells may use the eating of live lymphocytes as a way to "feed" in condition of low nutrient supply. The mechanism underlying cannibalism involved a complex framework, including lysosomal protease cathepsin B activity, caveolae formation, and ezrin cytoskeleton integrity and function. In conclusion, our study shows that human metastatic melanoma cells may eat live T cells, which are instead programmed to kill them, suggesting a novel mechanism of tumor immune escape. Moreover, our data suggest that cannibalism may represent a sort of "feeding" activity aimed at sustaining survival and progression of malignant tumor cells in an unfavorable microenvironment.
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PMID:Cannibalism of live lymphocytes by human metastatic but not primary melanoma cells. 1717 2

Delivery of cytokine genes at the tumor site in pre-clinical models has been shown to recruit host inflammatory cells followed by inhibition of tumor growth. This local effect is often accompanied by systemic protection mediated by the immune system, mainly by CD8(+) T and NK cells. On this basis, cytokine gene-transduced tumor cells have widely been used as vaccines in clinical trials, which have shown good safety profiles and some local responses but substantial lack of systemic efficacy. Are these findings the end of the story? Possibly not, if major improvements will be attained in the coming years. These should be directed at the level of gene selection and delivery, in order to identify the optimal cytokine and achieve efficient and durable cytokine expression, and at the level of improving immune stimulation, i.e. by co-administration of co-stimulatory molecules including B7 and CD40, or boosting the expression of tumor antigens or MHC class I molecules. Interestingly, some of the cytokines which have shown encouraging anti-tumor activity, including IFNs, IL-4, IL-12 and TNF-alpha, are endowed with anti-angiogenic or vasculotoxic effects, which may significantly contribute to local tumor control. Therapeutic exploitation of this property may result in the design of novel approaches which, by maximizing immune-stimulating and anti-angiogenic effects, could possibly lead to starvation of established tumors in patients.
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PMID:Angiogenesis meets immunology: cytokine gene therapy of cancer. 1730 60

Malnutrition compromises immune function, resulting in reduced resistance to infection. Recent animal and human studies have suggested that leptin is capable of modulating the immune response and that its levels, which are regulated by nutritional status, fall rapidly during starvation. Leptin deficiency is associated with impaired cell-mediated immunity, an increased incidence of infectious disease and an associated increase in mortality. The purpose of this study was to examine the effect of leptin on activation and cytokine production in peripheral blood T cells from malnourished children. The data obtained in the present study demonstrate that leptin produced an increase in the percentage of CD4(+) and CD8(+) cells producing interleukin (IL)-2 and interferon (IFN)-gamma in 24-h cultures. Moreover, leptin decreased the percentage of CD4(+) and CD8(+) cells producing IL-4 and IL-10, and enhanced activation of circulating T cells when co-stimulated by phorbol 12-myristate 13 acetate (PMA)-ionomycin. Leptin enhanced the expression of activation markers CD69 and CD25 in both CD4(+) and CD8(+) cells after 5 h of stimulation. In conclusion, the results obtained show that leptin modulates CD4(+) and CD8(+) cell activation towards a T helper 1 (Th1) phenotype by stimulating the synthesis of IL-2 and IFN-gamma. In contrast, leptin decreases IL-4 and IL-10 production. Moreover, leptin enhanced the expression of CD69 and CD25 on CD4(+) and CD8(+) cells after stimulation with PMA-ionomycin.
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PMID:Effect of leptin on activation and cytokine synthesis in peripheral blood lymphocytes of malnourished infected children. 1735 47

There is accumulating evidence to support the interactions between psychological stress and inflammatory bowel disease (IBD). In order to elucidate the relationship between psycoimmunological stress and IBD, we examined the alteration of immune system during the disease course of experimental Ulcerative colitis(UC)-model induced by dextran sulfate sodium (DSS). When C57BL/6 mice were treated with 4.5% DSS, they developed progressive weight loss. In contrast, the same treatment applied to BALB/c mice led to a small weight loss from which they soon recovered. Surprisingly, we found significant involution of the thymus and a reduction in the number of double positive thymocytes in DSS-treated C57BL/6 mice but not in DSS-treated BALB/c mice. Double negative thymocytes, especially DN1 (CD25-CD44+) and DN2 (CD25+CD44+) thymocytes, were relatively upregulated. The weights of spleens were slightly increased in both C57BL/6 and BALB/c mice following oral administration of DSS. In C57BL/6 spleens, both CD4 and CD8 single positive T cells gradually decreased (day 3), then recovered (day 14) after treatment. Because oral administration causes starvation, we examined the effects of starvation on the thymus and spleen. Although involution of thymus was observed both in starvation and DSS-treatment, the weight of spleen was reduced only in starvation. Also, the population changes in thymocytes in starvation was different from DSS-treatment. The administration of the steroid inhibitor RU486 partially reversed the thymic involution in C57BL/6 mice, thus DSS-treated UC might induce psycoimmunological changes partly through hypothalamic-pituitary-adrenal axis.
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PMID:Thymic involution correlates with severe ulcerative colitis induced by oral administration of dextran sulphate sodium in C57BL/6 mice but not in BALB/c mice. 1869 22

C57BL/6 (B6) mice are genetically highly susceptible to chronic type II Toxoplasma gondii infections that invariably cause lethal toxoplasmic encephalitis. We examined the ability of an attenuated type I vaccine strain to elicit long-term immunity to lethal acute or chronic type II infections in susceptible B6 mice. Mice immunized with the type I cps1-1 vaccine strain were not susceptible to a lethal (100-cyst) challenge with the type II strain ME49. Immunized mice challenged with 10 ME49 cysts exhibited significant reductions in brain cyst and parasite burdens compared to naive mice, regardless of the route of challenge infection. Remarkably, cps1-1 strain-immunized B6 mice chronically infected with ME49 survived for at least 12 months without succumbing to the chronic infection. Potent immunity to type II challenge infections persisted for at least 10 months after vaccination. While the cps1-1 strain-elicited immunity did not prevent the establishment of a chronic infection or clear established brain cysts, cps1-1 strain-elicited CD8(+) immune T cells significantly inhibited recrudescence of brain cysts during chronic ME49 infection. In addition, we show that uracil starvation of the cps1-1 strain induces early markers of bradyzoite differentiation. Collectively, these results suggest that more effective immune control of chronic type II infection in the genetically susceptible B6 background is established by vaccination with the nonreplicating type I uracil auxotroph cps1-1 strain.
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PMID:Long-term immunity to lethal acute or chronic type II Toxoplasma gondii infection is effectively induced in genetically susceptible C57BL/6 mice by immunization with an attenuated type I vaccine strain. 1979 73

Bis (Bag3) is known to be involved in cell survival, migration, the regulating of chaperones, and protein quality control. We reported recently on the production of bis gene-deleted mice, which show early lethality within 3 wk after birth with a phenotype showing severe malnutrition and shrinkage of the thymus. In this report, we provide evidence to show that an intrinsic problem of adrenal gland is the the primary cause for the severe atrophy of the thymus in bis(-/-) mice. The bis(-/-) mice show significantly higher levels of corticosterone, but CRH and ACTH levels were considerably lower than those of wild littermates. The transcription of steroidogenic enzymes was increased in the adrenal glands of bis(-/-) mice, accompanied by an increase in the thickness of the zona reticularis. An analysis of thymus tissue from bis(-/-) mice revealed that the severe atrophy of the thymus is due to the specific loss of immature double-positive (CD4(+)CD8(+)) cortical thymocytes by apoptosis, as evidenced by immunohistochemical examination and flow cytometric analysis, which were restored by injection of an inhibitor of glucocorticoid synthesis. In vitro cultures of thymocytes with increasing doses of dexamethasone exhibited a similar degree of apoptosis between wild and bis(-/-) thymocytes. The corticosterone levels from fasted wild littermates were one-half those of bis(-/-) mice, although serum glucose levels were similar. Thus, the deletion of the bis gene resulted in the intrinsic defect in the adrenal gland, leading to a marked increase in glucocorticoid levels, probably upon starvation stress, which accounts for the massive apoptosis of the thymus.
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PMID:Deletion of the bis gene results in a marked increase in the production of corticosterone that is associated with thymic atrophy in mice. 2154 Apr 52


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