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Results for “Immune function”

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At least 649 records · Page 36Linked to original sources
PubMed1996

Does fluoridation harm immune function?

There have been suggestions, mainly in the lay press, that fluoridation might affect immunity. Careful examination of various studies on fluoride and immune function do not support this suggestion. Whilst fluoride at high concentrations can have inhibitory effects on lymphocyte and polymorphonuclear leucocyte function, these concentrations are many times higher than levels which would be expected from fluoridation. Fluoride can act as an immunological adjuvant. There is no evidence of any deleterious effect on specific immunity following fluoridation nor any confirmed reports of allergic reactions.

Adjuvants, Immunologic↗
PubMed1996

Effects of supplemental dietary arginine, canola oil, and trace elements on cellular immune function in critically injured patients.

Dietary nutrients may have pharmacological value in modulating the immune system. We studied the effects of two enteral diets, which differed in their content of arginine, fat source, and select trace elements, on immune function in critically injured patients. Leukocytes were isolated from healthy volunteers and severely injured (ISS > 13) patients on the first, sixth, and tenth day of receiving either a standard diet or experimental diet. Monocytes were assayed for tumor necrosis factor, procoagulant activity, and prostaglandin E2 following endotoxin exposure. Neutrophil oxidant production and lymphocyte blastogenesis was assessed. Leukocyte function was uniformly depressed compared to normal patients on day 1. The response of leukocytes from patients receiving experimental diet improved or "normalized" by day 6, while remaining depressed in patients receiving standard diet. Dietary nutrient modification can effect cellular immune responses to inflammatory stimuli in severely injured patients.

Adolescent↗
PubMed2003

Nocturnal catecholamines and immune function in insomniacs, depressed patients, and control subjects.

Insomnia predicts cardiovascular and non-cardiovascular disease mortality. This study evaluated EEG sleep, nocturnal sympathetic activity, and daytime measures of immune function in subjects with primary insomnia (n = 17) and patients with current major depression (n = 14) as compared to controls (n = 31). Insomniacs showed disordered sleep continuity along with nocturnal increases of average levels of circulating norepinephrine and decreases of natural killer cell responses, whereas depressed patients showed declines of natural killer cell activity, but no differences of EEG sleep or nocturnal catecholamines as compared to controls. Impairments of sleep efficiency correlated with nocturnal elevations of norepinephrine in the insomniacs but not in the depressives or controls. These data indicate that insomnia is associated with nocturnal sympathetic arousal and declines of natural immunity, and further support the role of sleep in the regulation of sympathetic nervous and immune system functioning.

Analysis of Variance↗
PubMed2001

Control of glial immune function by neurons.

The immune status of the central nervous system (CNS) is strictly regulated. In the healthy brain, immune responses are kept to a minimum. In contrast, in a variety of inflammatory and neurodegenerative diseases, including multiple sclerosis, infections, trauma, stroke, neoplasia, and Alzheimer's disease, glial cells such as microglia gain antigen-presenting capacity through the expression of major histocompatibility complex (MHC) molecules. Further, proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF), interleukin-1beta (IL-1beta), and interferon-gamma (IFN-gamma), as well as chemokines, are synthesized by resident brain cells and T lymphocytes invade the affected brain tissue. The proinflammatory cytokines stimulate microglial MHC expression in the lesioned CNS areas only. However, the induction of brain immunity is strongly counterregulated in intact CNS areas. For instance, recent work demonstrated that microglia are kept in a quiescent state in the intact CNS by local interactions between the microglia receptor CD200 and its ligand, which is expressed on neurons. Work done in our laboratory showed that neurons suppressed MHC expression in surrounding glial cells, in particular microglia and astrocytes. This control of MHC expression by neurons was dependent on their electrical activity. In brain tissue with intact neurons, the MHC class II inducibility of microglia and astrocytes by the proinflammatory cytokine IFN-gamma was reduced. Paralysis of neuronal electric activity by neurotoxins restored the induction of MHC molecules on microglia and astrocytes. Loss of neurons or their physiological activity would render the impaired CNS areas recognizable by invading T lymphocytes. Thus, immunity in the CNS is inhibited by the local microenvironment, in particular by physiologically active neurons, to prevent unwanted immune mediated damage of neurons.

Animals↗
PubMed1989

Soluble extracts from larval Ostertagia ostertagi modulating immune function.

BALB/c mice were immunized with Ostertagia ostertagi antigens and keyhole limpet hemocyanin (KLH) or sheep erythrocytes (SR) for evaluation of antibody production by enzyme linked immunosorbent assay (ELISA) or modified Jerne plaque assay. One semi-purified larval antigen caused both decreased anti-KLH serum antibody levels and fewer anti-SR IgM-secreting B cells. This antigen was shown to depress lymphocyte blastogenesis to Concanavalin A when added to cultured BALB/c splenic lymphocytes.

Animals↗
PubMed2006

Hypothalamic integration of immune function and metabolism.

The immune and neuroendocrine systems are closely involved in the regulation of metabolism at peripheral and central hypothalamic levels. In both physiological (meals) and pathological (infections, traumas and tumors) conditions immune cells are activated responding with the release of cytokines and other immune mediators (afferent signals). In the hypothalamus (central integration), cytokines influence metabolism by acting on nucleus involved in feeding and homeostasis regulation leading to the acute phase response (efferent signals) aimed to maintain the body integrity. Peripheral administration of cytokines, inoculation of tumor and induction of infection alter, by means of cytokine action, the normal pattern of food intake affecting meal size and meal number suggesting that cytokines acted differentially on specific hypothalamic neurons. The effect of cytokines-related cancer anorexia is also exerted peripherally. Increase plasma concentrations of insulin and free tryptophan and decrease gastric emptying and d-xylose absorption. In addition, in obesity an increase in interleukin (IL)-1 and IL-6 occurs in mesenteric fat tissue, which together with an increase in corticosterone, is associated with hyperglycemia, dyslipidemias and insulin resistance of obesity-related metabolic syndrome. These changes in circulating nutrients and hormones are sensed by hypothalamic neurons that influence food intake and metabolism. In anorectic tumor-bearing rats, we detected upregulation of IL-1beta and IL-1 receptor mRNA levels in the hypothalamus, a negative correlation between IL-1 concentration in cerebro-spinal fluid and food intake and high levels of hypothalamic serotonin, and these differences disappeared after tumor removal. Moreover, there is an interaction between serotonin and IL-1 in the development of cancer anorexia as well as an increase in hypothalamic dopamine and serotonin production. Immunohistochemical studies have shown a decrease in neuropeptide Y (NPY) and dopamine (DA) and an increase in serotonin concentration in tumor-bearing rats, in first- and second-order hypothalamic nuclei, while tumor resection reverted these changes and normalized food intake, suggesting negative regulation of NPY and DA systems by cytokines during anorexia, probably mediated by serotonin that appears to play a pivotal role in the regulation of food intake in cancer. Among the different forms of therapy, nutritional manipulation of diet in tumor-bearing state has been investigated. Supplementation of tumor bearing rats with omega-3 fatty acid vs. control diet delayed the appearance of tumor, reduced tumor-growth rate and volume, negated onset of anorexia, increased body weight, decreased cytokines production and increased expression of NPY and decreased alpha-melanocyte-stimulating hormone (alpha-MSH) in hypothalamic nuclei. These data suggest that omega-3 fatty acid suppressed pro-inflammatory cytokines production and improved food intake by normalizing hypothalamic food intake-related peptides and point to the possibility of a therapeutic use of these fatty acids. The sum of these data support the concept that immune cell-derived cytokines are closely related with the regulation of metabolism and have both central and peripheral actions, inducing anorexia via hypothalamic anorectic factors, including serotonin and dopamine, and inhibiting NPY leading to a reduction in food intake and body weight, emphasizing the interconnection of the immune and neuroendocrine systems in regulating metabolism during infectious process, cachexia and obesity.

Adipose Tissue↗
PubMed2001

Bacterial translocation and immunohistochemical measurement of gut immune function.

AIMS: The local immune response in the small bowel mucosa might play a role in bacterial translocation (BT). The aim of this study was to quantify immune cells and secretory antibodies in the small bowel mucosa, and relate this to BT as assessed by culture of a mesenteric lymph node. METHODS: Immunohistochemical techniques were used to measure the frequency of plasma cells and IgA and IgM positive cells in the lamina propria and semiquantitatively to assess mucosal surface IgA and IgM values in small bowel specimens obtained from 11 patients in whom positive evidence of BT had been identified in a mesenteric lymph node harvested at the time of laparotomy. These were compared with similar specimens obtained from 11 patients in whom a similar lymph node had yielded no growth. RESULTS: BT was associated with a significantly increased median frequency of plasma cells (p < 0.01) and IgA positive cells (p < 0.05) in the lamina propria. The frequency of IgM positive cells was also higher in these patients, although this difference was not significant. In addition, semiquantitatively scored IgA and IgM concentrations at the mucosal surface were both significantly higher in the patients in whom BT had been identified (p = 0.006 and 0.016, respectively). CONCLUSION: Higher numbers of plasma cells and higher IgA and IgM values are present in the small bowel mucosa of patients in whom BT has been shown to occur, suggesting an increased local immune response.

Aged↗
PubMed1987

The effects of ultraviolet irradiation of the skin on herpes simplex virus infection: alteration in immune function mediated by epidermal cells and in the course of infection.

Previously, we demonstrated that Ia+ epidermal cells (EC) have herpes simplex virus (HSV) antigen-presenting capacity in vitro and play an important role in resistance to HSV infection in vivo. In the present study, we investigated the effects of in vivo ultraviolet (UV) irradiation of the skin on the HSV-immunity function of EC both in vitro and in vivo and on the pathogenesis of HSV infection. Immune T cells cultured with EC and HSV antigen showed a proliferative response in vitro. Exposure of the skin to UV light 1 to 3 days before preparation of EC resulted in dose-dependent impairment of this proliferation. This UV-induced impairment of the accessory cell function of EC was accompanied by a parallel reduction of the number of Ia+ EC. We also transferred these EC-stimulated T cells to intracutaneously infected nude mice. Immune T cells stimulated with EC obtained from irradiated mice did not effectively clear HSV and allowed development of zosteriform skin lesions. In contrast normal-EC-stimulated immune T cells completely prevented the formation of a zosteriform rash. In addition, mice irradiated with UV on shaved midflank skin 2 days before intracutaneous inoculation of HSV showed increased severity of infection and a higher incidence of latency compared with control mice. These studies indicate that in vivo UV irradiation of the skin abrogates the immune function of EC both in vitro and in vivo, and affects HSV pathogenesis. The implication of our results for the better understanding of the effect of UV on acute and recurrent HSV infections is discussed.

Animals↗
PubMed1999

Immune function of the upper splenic remnant supplied by short gastric vessels.

OBJECTIVE: To study the immune function of the upper third of the spleen supplied by short gastric vessels after two thirds partial splenectomy. DESIGN: Experimental study. SETTING: Teaching hospital, Turkey. MATERIAL: Sixty Wistar-albino rats, 20 in each group. INTERVENTIONS: Control = sham laparotomy; partial splenectomy = the upper third of the spleen supplied by short gastric vessels was preserved after two thirds partial splenectomy and dividing the main vascular supply; and total splenectomy. At the end of the sixth week postoperatively, antigenic stimulation was induced with an injection of pneumococcal suspension in 10 animals from each group. 0.5 ml of diluted Indian ink was injected into the aorta. MAIN OUTCOME MEASURES: Histological architecture of splenic tissue, and changes in the white pulp after antigenic stimulus. Bacteriological analysis with aerobic blood culture. Phagocytic activity as counted by Indian-ink-laden macrophages. The ability to produce antibodies as measured by serum IgM concentrations. RESULTS: Histological architecture of splenic tissue was normal. Germinal centres (p = 0.02), lymphoid follicles (p = 0.09), and their ratio (p = 0.0006) in the white pulp of the splenic remnant was significantly increased after antigenic stimulus compared with normal spleen. Significantly more animals without spleens developed bacteraemia (p = 0.02). Phagocytic activity of the upper splenic remnant was 89% that of normal spleen. Serum IgM concentrations without antigenic stimulus were 144, 138.2 (p = 0.6), and 86.2 (p < 0.001) mg/L; and with antigenic stimulus 263, 201.7 (p < 0.0001), and 98.1 (p < 0.0001) mg/L in groups 1, 2, and 3, respectively. The increase in serum IgM concentrations as a response to antigen was significant in the control (p < 0.0001) and in the partial splenectomy group (p < 0.0001), but not in the splenectomy group (p = 0.1). CONCLUSIONS: After reduction of its volume, the upper splenic remnant remained adequately supplied by the short gastric vessels. The upper part of the spleen preserved its normal histological architecture, had considerable phagocytic activity, possessed the ability to produce antibodies, and created a satisfactory immune response to antigenic stimulus. In rats, a considerable volume of functional and well perfused splenic tissue is preserved even after dividing the main vessels.

Animals↗
PubMed1991

Effects of rat cytomegalovirus infection on immune functions in rats with collagen induced arthritis.

The effect of rat cytomegalovirus (CMV) infection on immune function was studied in rats with collagen induced arthritis, an experimental model of autoimmunity targeted to cartilage and previously shown to be greatly augmented in severity by rat CMV. Rat CMV infection induced an early (7 to 14 day), 2.5-fold increase in circulating B cells (SIgG+) which was associated with moderate increases in the titers of serum IgG antirat type II collagen antibody. A significantly increased skin test reactivity (p less than 0.025) to rat type II collagen was detected at Day 14 and followed a small increase in numbers of W3/25+ T-helper cells in peripheral blood noted at Day 8. A 3-fold expansion of OX8+ peripheral lymphocytes, occurring maximally at Day 8, was tentatively identified as a natural killer cell population by functional 51Cr-release assays. Our data indicate that rat CMV augmentation of collagen induced arthritis is associated with a generalized but modest increase in immune reactivity towards rat type II collagen and with significant alterations of peripheral lymphocyte subsets.

Animals↗
PubMed1998

[Study on the cellular immune function and cytokines in aplastic anemia patients].

OBJECTIVE: To evaluate the effects of cellular immune function and cytokines on the pathogenesis of aplastic anemia (AA) and its clinical significance. METHODS: T lymphocyte subsets and HLA-DR antigen expression in the peripheral blood cells were assayed, and the levels of G-CSF, IL-6, TNF alpha, IFN alpha and IL-8 in the PBMNC culture supernatants were determined in 38 AA patients and 20 normal control with APAAP and ELISA methods. RESULTS: CD4+ cells, CD4+/CD8+ cells and G-CSF level were lower, and CD8+ cells, HLA-DR+ cells and IL-6, TNF alpha, IFN alpha and IL-8 levels were higher in AA patients than in normal controls. The level of G-CSF was positively correlated with CD4+ cells and CD4+/CD8+ cells and negatively with IFN alpha level. IL-6 level was negatively correlated with WBC count and CD4+ cells. TNF alpha level was positively correlated with CD8+ cells and negatively with CD4+/CD8+ cells. IL-8 level was positively correlated with CD8+ cells and HLA-DR+ cells. CONCLUSION: The cellular immune dysfunction and cytokine aberration participate in the pathogenesis of AA.

Adult↗
PubMed1996

[Determinations of antiovarian antibodies and cellular immunity functions in patients with premature ovarian failure].

OBJECTIVE: To investigate the variations of cellular immunity function and its relationship with antiovarian antibodies (AOAb) in patients with premature ovarian failure (POF). METHODS: Serum AOAb, T-lymphocyte subsets and leukocyteprocoagulant activity (LPCA) to ovarian antigens of peripheral blood were examined in 30 normal women (control group) and 30 patients with POF (POF group). RESULTS: The mean serum AOAb level in POF group was significantly higher than that in control group (6.80 +/- 1.9 kU/L vs 1.39 +/- 0.72 kU/L, P < 0.01). The percentage of CD3+, CD4+ cells increased significantly (65.42 +/- 5.31% and 44.79 +/- 5.90%, respectively), the percentage of CD8- cells was significantly lower (25.63 +/- 4.26%) and the ratio of CD4+/CD8+ increased (1.66 +/- 0.27) in POF group when compared with control group (P < 0.01). The positive rate of AOAb in patients who had elevated ratio of CD4+/CD8+ was significantly higher than those with normal CD4+/CD8+ ratio (85.7%, 18/21 vs 3/9; P < 0.01). The level of LPCA was elevated in POF patients with positive AOAb, and was correlated positively with the level of AOAb (chi 2 = 8.378, P < 0.01). CONCLUSIONS: These data showed that cellular immunity and humoral immunity to ovarian antigens can be concurrently produced in POF patients, and suggested that pathogenesis of POF may be associated with immune factors.

Adult↗
PubMed1982

Immune function in the malnourished host.

Deficiencies of protein, energy, and specific vitamins and minerals impair function of various components of the immunological network and therefore weaken host defense. These various deficiencies may affect specific loci within the network, but because of the interrelations between the different systems, the ultimate effect may be quite broad. Patients with PEM often suffer infections, which may also impair the immune function. It is difficult to separate effects of malnutrition from those of infection, a fact recognized in the recent coinage of the term malnutrition-infection complex. On the basis of the available information it appears that PEM and associated deficiencies of nutrients cause a major impairment in the T lymphocytes and the complement system. They have relatively less effect on the B lymphocytes and the phagocytes directly; however, normal B cell activity is dependent on regulatory influences of T cells and the phagocytic cells require mediators generated from the activation of complement. Therefore these cells also are functionally defective in PEM. The consequence of these deficiencies of function of the immune system in the malnourished host is heightened susceptibility to and a less vigorous response to infections. These defects can be generally reversed by nutritional rehabilitation.

Antibody Formation↗
PubMed2003

Effect of dietary ascorbyl-2-phosphate on immune function after transport to a feeding facility.

Effects of dietary ascorbyl-2-phosphate on immune function after a 210-km trip were measured in 18 Holstein heifers. After transport on d 0, 10 g of ascorbyl-2-phosphate each were added to the diets of 10 heifers, whereas eight heifers were fed a control diet. Plasma cortisol concentrations increased by an average of 25.6 microgram/ml on d 0 following transport, but by d 7 after transport had decreased to pretransport levels. Average daily gain was lower in heifers fed ascorbyl-2-phosphate from d 28 to 49 d after transport, but did not differ over the entire study. Feeding ascorbyl-2-phosphate maintained plasma ascorbate concentrations on d 7 post-transport, which decreased in control heifers. Plasma keyhole limpet hemocyanin antibody titers were significantly higher in control heifers from d 7 to 49. Mononuclear leukocyte proliferation responses were decreased on d 0 in lymphocytes stimulated by mitogens, with pokeweed mitogen-stimulated cells showing less of a response than cells stimulated by the other mitogens. In the absence of mitogens, dietary ascorbyl-2-phosphate increased basal 3H-methyl thymidine incorporation by cultured lymphocytes. Across diets and mitogens, lymphocytes treated with cortisol showed decreased 3H-methyl thymidine incorporation. Transportation acted as a stressor, as evidenced by the increased plasma cortisol levels at d 0 immediately after transport, but immunological effects were not apparent by d 7. Feeding ascorbyl-2-phosphate maintained plasma ascorbate concentrations on d 7, but had negative effects on immune responses posttransport.

Animals↗
PubMed1983

Thymus-dependent immune functions in chickens bursectomized with colchicine applied to the anal lips.

Thymus-dependent immune functions were investigated in chickens bursectomized neonatally with colchicine solution given per anum. Antibody responses to thymus-dependent antigens sheep red blood cells (SRBC) and human gamma-globulin (HGG) were delayed, reaching the normal level after the third antigen stimulation. Also the mitogenic responses of peripheral blood lymphocytes were preserved, and no changes in the thymic morphology were found. In contrast, antibody responses to bursa-dependent antigen Brucella abortus were low and the switch of immunoglobulin isotypes from IgM to IgA and IgG was disturbed. It can be concluded that neonatal bursectomy with cloacal administration of colchicine does not significantly affect T cell functions, whereas B cell functions are partially deficient.

Animals↗
PubMed1982

In vivo and in vitro effects of 1,1-dimethylhydrazine on selected immune functions.

The in vivo phase of the experiments reported here include the evaluation of immune function after short-or long-term treatment of mice with 1,1-dimethylhydrazine (UDMH). Long-term exposure (3 injections/week for 14 weeks) resulted in increased numbers of Jerne plaque-forming cells, a trend toward decreased induction of suppressor cell activity by concanavalin A (Con A), and no effects on mitogen-induced lymphocyte blast transformation (LBT), compared to saline-treated control mice. These effects were greatest at doses of 10 or 50 mg/kg, while higher doses had less of an effect. In vitro experiments were performed by adding UDMH to normal murine splenocytes in the LBT assay and con A-induced suppressor cell assay. The UDMH induced a significant enhanced response to lipopolysaccharide (LPS) at 10 and 50 micrograms/ml, and a suppressed response to both Con A and LPS at higher concentrations. The UDMH also caused a decrease in suppressor cell activity at 25 micrograms/ml. Selective abrogation of suppressor activity or alteration of the suppressor cell-helper ratio were suggested as possible mechanisms for the enhancement effect associated with UDMH.

Animals↗
PubMed1985

In vitro evidence for defective afferent immune function in long-term renal allograft recipients.

Experiments were designed to evaluate afferent immune functions in 21 long-term (greater than or equal to 3 years) renal allograft recipients by using in vitro assays that included autologous and allogeneic mixed lymphocyte reactions (AMLR and allo-MLR), proliferative responses to a soluble antigen (tetanus toxoid), and the ability to generate cytotoxic T lymphocytes (CTL) following stimulation in an AMLR. The results showed that allograft recipients generated responses in the allo-MLR (means = 84,789 +/- 8242) that were comparable to those exhibited by normal controls (means = 86,082 +/- 7423). Likewise, mean responses in the AMLR were similar in recipients and controls (14,937 +/- 3243 versus 16,101 +/- 3005), although a greater percentage of recipients generated AMLRs below 5000 cpm than did normals (8/21 versus 4/20). However, 13 recipients analyzed for responsiveness to tetanus toxoid were shown to generate mean proliferative responses that were significantly depressed below normal (18,095 +/- 5545 versus 48,935 +/- 8813, P less than 0.001). Furthermore, despite significant proliferation in the AMLR means = 27,648 +/- 5168), 8 recipients generated significantly lower CTL activity in AMLR cultures than normal controls (mean percentage of cytotoxicity = 10.3 +/- 4.7 versus 24.9 +/- 4.7, P less than 0.05). These recipients generated normal CTL levels against allogeneic target cells following stimulation in an allo-MLR. Thus, these studies provide experimental support for the existence of altered T helper cell-mediated functions in long-term renal allograft recipients.

Humans↗