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PubMedDate not supplied

Cellular immune functions, endorphins, and alcohol consumption in males.

The effects of alcohol abuse on cellular immune functions were measured by various levels of alcohol use in adult men. Total lifelong abstainers were used as controls. Previous abusers, current abusers, and patients with alcoholic cirrhosis or pancreatitis were age-matched to controls. T-lymphocyte mitogenesis stimulated by phytohemagglutinin and concanavalin A was generally reduced in peripheral blood lymphocytes of current and previous alcohol consumers, although the decrease was not statistically significant. B-cell mitogenesis stimulated by pokeweed mitogen was not changed by previous alcohol consumption. The number of T-cells was not changed by either previous or current alcohol abuse. T-helper cells were significantly increased and T-suppressor cells increased only in the patients with alcoholic cirrhosis or pancreatitis. The percentage of T-lymphocytes with T-suppressor characteristics in controls was 27% while in alcoholic cirrhosis or pancreatitis subjects it was 16%. Plasma corticosteroid levels were significantly increased in people currently consuming alcohol (12.1 +/- 1.1 mg/dl) compared to controls (7.7 +/- 1.1). The corticosteroid levels were also higher in previous alcohol abusers although not statistically significant. Plasma endorphin levels were increased by severe alcohol abuse in the patients with cirrhosis or pancreatitis to 25.03 +/- 6.74 from 11.85 +/- 2.48 pg/ml in controls.

Adult↗
PubMed1989

The effect of antidepressants on immune function in mice.

Depression or its treatment with antidepressant agents may have an impact on the normal function of the immune system. To address this issue in an animal model, we studied the effect of maprotiline and desipramine treatment of mice on several immunological activities associated with host resistance to cancer and infections. Our results indicate that chronic maprotiline treatment depressed natural killer (NK) cell function, measured in vivo as clearance of tumor cells from the lung or in vitro as cytolytic activity. Cell-mediated immunity, measured as delayed hypersensitivity in vivo and T and B lymphocyte proliferative responses in vitro, was largely unaffected. Although antidepressant toxicity at high concentrations inhibited T, B, and NK cell activity, it is unlikely that this is the basis for the in vivo effects.

Animals↗
PubMed1994

[Relationship between nutritional depletion and cell-mediated immune function in active pulmonary tuberculosis].

A survey on the nutritional status and cell-mediated immune function of 47 hospitalized patients with active pulmonary tuberculosis and healthy controls was conducted. In the patients group: 1) Anthropometric measurements, such as %ideal body weight (%IBW), %arm circumference (%AC), %arm muscle circumference (%AMC) and %triceps skin fold (%TSF), were significantly reduced. 2) Visceral proteins including serum albumin (Alb), transferrin (Tf), prealbumin (PA) and retinol binding protein (RBP) were significantly reduced. 3) The imbalance of plasma amino acids, which was characterized by the depression of Fischer ratio, a molar ratio of branched chain amino acids (BCAA) to aromatic amino acids (AAA), was observed. Fischer ratio was significantly correlated with anthropometric measurements (%IBW, %AC and %AMC). Delayed-type hypersensitivity to DNCB (2,4-dinitrochlorobenzene) and lymphocyte transformation to phytohemagglutinin (PHA) and concanavalin A (Con A) were significantly impaired in the patients group, whereas NK cell activity was higher than that of controls. Alb, PA, RBP and Fischer ratio were significantly lower in the patients with reduced DNCB reaction than in those with normal responses. Lymphocyte transformation was significantly correlated with Fischer ratio, and NK cell activity was significantly correlated with Alb, PA, RBP. These data may suggest that the imbalance of plasma amino acids represented by the reduction of Fischer ratio and the depletion of visceral proteins are closely related to the impairment of lymphocyte function in the patients with active pulmonary tuberculosis.

Adult↗
PubMed2000

Review of immune function, healing of pressure ulcers, and nutritional status in patients with spinal cord injury.

The immune, neural, and endocrine systems do not act autonomously; rather, multiple communicative pathways exist among the nervous, endocrine, and immune systems that facilitate physiological immunoregulation. Patients with spinal cord injury (SCI) have decreased natural and adaptive immune responses by 2 weeks after injury. In patients with SCI, adrenocorticotropic hormone (ACTH) and urine-free cortisol levels were increased while zinc and albumin levels were decreased, respectively. In addition, the surface markers alpha 2, alpha 3, alpha 4, CD11a, CD11b, CD18, CD54, and CD8 found on lymphocytes and alpha 3, alpha 4, CD11a, CD18, and CD8 surface markers found on granulocytes were also decreased in the patient population. Finally, the adhesion molecules binding ability in the SCI group was also decreased when compared with a control group. Overall, the investigation showed that patients with SCI have a decreased immune function, especially succeeding the SCI injury, an impaired nutrition status, and a decreased number of adhesion molecules, all of which contribute to delayed wound healing.

Adult↗
PubMed1994

Central nervous system and peripheral immune functions and the sleep-wake system.

This paper reviews the relationship of aspects of the immune system to the sleep-wake system in animals and humans. In addition to the influence of certain cytokines such as interleukin-1 (IL-1) on the sleeping-waking brain, circadian measures of plasma IL-1 and peripheral immune cellular functions, for example, natural killer cell activities and cortisol are related to the sleep-wake system in humans. Changes in the circadian patterns of immune functions over the menstrual cycle are associated with the amount of progesterone and slow wave sleep. The harmonious inter-relationship of the circadian pattern of the immune, endocrine and sleep-wake systems may be important in the cause and functions of sleep.

Animals↗
PubMed2006

Differential regulation of metabolic, neuroendocrine, and immune function by leptin in humans.

To elucidate whether the role of leptin in regulating neuroendocrine and immune function during short-term starvation in healthy humans is permissive, i.e., occurs only when circulating leptin levels are below a critical threshold level, we studied seven normal-weight women during a normoleptinemic-fed state and two states of relative hypoleptinemia induced by 72-h fasting during which we administered either placebo or recombinant methionyl human leptin (r-metHuLeptin) in replacement doses. Fasting for 72 h decreased leptin levels by approximately = 80% from a midphysiologic (14.7 +/- 2.6 ng/ml) to a low-physiologic (2.8 +/- 0.3 ng/ml) level. Administration of r-metHuLeptin during fasting fully restored leptin to physiologic levels (28.8 +/- 2.0 ng/ml) and reversed the fasting-associated decrease in overnight luteinizing hormone pulse frequency but had no effect on fasting-induced changes in thyroid-stimulating hormone pulsatility, thyroid and IGF-1 hormone levels, hypothalamic-pituitary-adrenal and renin-aldosterone activity. FSH and sex steroid levels were not altered. Short-term reduction of leptin levels decreased the number of circulating cells of the adaptive immune response, but r-metHuLeptin did not have major effects on their number or in vitro function. Thus, changes of leptin levels within the physiologic range have no major physiologic effects in leptin-replete humans. Studies involving more severe and/or chronic leptin deficiency are needed to precisely define the lower limit of normal leptin levels for each of leptin's physiologic targets.

Adaptation, Physiological↗
PubMed1986

Effect of tamoxifen on immune functions.

Tamoxifen (20 mg twice daily) was given to ten patients with breast cancer whose immune functions were determined prior to and 3, 6, and 12 months after starting tamoxifen therapy. No consistent changes could be observed in erythrocyte rosette-forming cell counts, erythrocyte antibody rosette-forming cells, active erythrocyte rosette-forming cells, theophylline-resistant rosette-forming cells, surface immunoglobulin-positive cells, and responses to mitogens phytohemagglutinin and concanavalin A. Erythrocyte antibody rosette-forming cells decreased significantly, however, at 6 months and active erythrocyte rosette-forming cells at 12 months after starting tamoxifen. We conclude that no change in the immune capacity could be detected during tamoxifen treatment.

Breast Neoplasms↗
PubMed1995

Effects of naltrexone on morphine-induced tolerance and physical dependence and changes in cellular immune function in mice.

The effects of naltrexone on tolerance/dependence, as well as alterations in cellular immune function induced by morphine administration, were determined. Mice were rendered tolerant to and physically dependent on morphine by subcutaneous implantation of pellets containing 75 mg of morphine. Implantation of naltrexone pellets (10 mg) blocked the development of tolerance to the analgesic action of morphine, as well as the development of physical dependence. Morphine suppressed lymphoid organ weights and cellularities, and this suppression was blocked by naltrexone. B-Cell proliferation was suppressed in morphine-tolerant but not in morphine-abstinent mice, and this suppression was exacerbated by naltrexone. Morphine tolerance and abstinence were associated with suppression of IL-2 production, which was completely blocked by naltrexone. NK cell activity was not significantly affected by either morphine or naltrexone exposure. The results suggest that the effects of morphine on the immune system are at least partially mediated through opioid receptors.

Animals↗
PubMed1994

The immune function and measles virus infection in three different socioeconomic child populations in Karachi, Pakistan.

The immune function as well as anti-measles virus antibody level were investigated with 111 children in Karachi who were classified into high-, middle- and low-income groups. No difference in the blood cell counts or the biochemical data among three groups indicates no marked difference in the general health conditions among them. In the low-income group, levels of IgG, IgA and anti-measles virus antibody were significantly higher than those in the other two groups. Although 30% of children of the low-income group kept extremely high levels of immunoglobulin, no significant correlation was observed between IgG levels and anti-measles virus antibody levels. In the high-income group, the level of IgM was significantly lower and the incidence of anti-measles virus antibody-negative children was high (7/38; 18.4%). These antibody-negative children kept lower immunoglobulin levels although they were over four years old. These results suggest that the living environmental conditions of these different socioeconomic groups vary greatly and hygienic conditions must influence the chance of encountering infectious pathogens including measles virus. The relation between living environment and risk of subacute sclerosing panencephalitis (SSPE) in child population of Krachi is discussed.

Antibodies, Viral↗
PubMed1992

The prostaglandin E1 analogue, misoprostol, regulates inflammatory cytokines and immune functions in vitro like the natural prostaglandins E1, E2 and E3.

We examined whether some immune functions related to the action and production of cytokines could be regulated by the natural prostaglandins E (PGE) and the PGE1 (ester) analogue, Misoprostol. PGE1,2,3 and Misoprostol inhibited: (1) the mitogenic activity of interleukin-1 (IL-1) for mouse thymocytes; (2) spreading of mouse macrophages on glass; (3) tumour necrosis factor (TNF) (alpha and beta) production by human peripheral blood mononuclear cells and rat macrophages; (4) IL-1 production by rat and mouse peritoneal macrophages; and (5) interferon-gamma (IFN-gamma) production by human peripheral blood mononuclear cells. These PGE had little effect on IL-1 production by human monocytes. By contrast, they all enhanced IL-6 production by rat and mouse macrophages and human monocytes. These effects were noted at concentrations below 500 nM (even as low as 10 nM). The relative potency of the prostanoids tested for both inhibitory and stimulatory effects was PGE1 = PGE2 = or greater than PGE3 greater than Misoprostol greater than PGA2 much greater than PGF1-alpha = PGF2-alpha = PGD2 (no effect). There is strong evidence that PGE1,2,3 and Misoprostol bind to the same receptor(s) and trigger the second messenger, cAMP, since dibutyryl cAMP (a lipophilic analogue of cAMP) had the same effects as the PGE. These PGE also induced elevated intracellular cAMP levels in and competed with [3H]PGE2 for binding to human and rat cells with the same relative potencies as described above.

Animals↗
PubMed1998

Improvement in cell-mediated immune function during potent anti-human immunodeficiency virus therapy with ritonavir plus saquinavir.

Inhibiting human immunodeficiency virus (HIV) replication with potent antiretroviral therapy may result in improved immune function, and this may lead to favorable outcomes, independent of changes in CD4+ lymphocyte count. The effect of combination protease inhibitor therapy (ritonavir plus saquinavir) on functional measures of cell-mediated immunity in 41 HIV-infected patients from one center of a multicenter trial was investigated. After 24 weeks, median plasma virus load decreased from 4.74 log10 copies/mL to below the detection limit of the assay (2.30 log10), and mean CD4+ lymphocyte count increased from 284 cells/microL to 413 cells/microL. Proliferative responses to phytohemagglutinin developed in 21 of 34 patients in whom responses were absent at baseline. Increases were observed in interleukin-2, -12, and -10 production and in the expression of CD28 on CD8+ lymphocytes. Initiation of potent anti-HIV therapy results in a degree of immune restoration, suggesting that HIV-induced immune suppression is a dynamic and potentially reversible process.

CD28 Antigens↗
PubMed1986

Adjuvant chemoimmunotherapy of cancer: influence of tumor burden and role of functional immune effector cells in mice.

Starting from the observation that success of combined treatment of MBL-2 tumor-bearing mice with the alkylating agent cyclophosphamide (CY; 150 mg/kg) and the immunomodulator maleic anhydride divinyl either copolymer (MVE-2; 25 mg/kg) was dependent upon a 1-3-day interval between treatment with CY and MVE-2, we have further analyzed in vitro and in vivo the relationship between tumor burden and the activity of immune effector cells in an adjuvant chemoimmunotherapy setting with CY and MVE-2. Treatment of MBL-2 tumor-bearing mice with CY (50-200 mg/kg) caused a dose- and time-dependent decrease in the i.p. tumor burden, which correlated with a significant increase in their median survival time. CY increased also the sensitivity of the residual MBL-2 tumor cells to Mø-mediated immunotherapy. The therapeutic efficacy of Mø-mediated immunotherapy with MVE-2, however, was restricted due to adverse effects of CY on the host's immune and hematopoietic functions. The time sequence with which these CY related positive effects on tumor burden and s(Tu)I, as well as the adverse effects on macrophages and hematopoietic functions occurred, gives sufficient explanation for the narrow window in time for successful immunotherapy with MVE-2 after preceding chemotherapy with CY. We therefore propose to modify the conventional chemoimmunotherapy of MBL-2 tumor-bearing mice by combining it with an intermittent in vivo transfer of in vitro cultivated Mø (therapy sequence: CY----Mø transfer----MVE-2), which would result in an increased Mø:MBL-2 tumor cell ratio at the site of the tumor while reducing the adverse effects of CY on macrophage functions.

Animals↗
PubMed2001

Pineal modulation of thymus and immune function in a seasonally breeding tropical rodent, Funambulus pennanti.

The immune system driven by cytokines is now known to be influenced by various other endocrine glands and its hormones. Results of the present study indicate a bidirectional relation between the pineal-thymus axis and the immune system status of an Indian tropical rodent, Funambulus pennanti, during winter months (reproductive inactive phase), when it faces maximum challenges from nature. Pinealectomy during the reproductive inactive phase inhibited thymus and spleen functions, which resulted in significant changes in leukocyte and lymphocyte counts and T-cell-mediated immune function (measured in terms of delayed-type hypersensitivity response to oxazolone). Blastogenic responses of lymphoid cells (thymocytes, splenocytes, and lymph node cells) also decreased following ablation of the pineal gland. To check the definite role of the pineal gland we injected melatonin into pinealectomized squirrels, and the suppressed immune function was significantly restored. Neuroendocrine control of the pineal gland on the histocompatible tissues in this seasonal breeder, F. pennanti, suggests an adaptive mechanism of the immune system for survival in the tropical zone. J. Exp. Zool. 289:90-98, 2001.

Animals↗
PubMed1981

[The effect of anaesthesia and surgery on immune function. A review (author's transl)].

This paper reviews the literature concerning the question, how the immune functions might be affected by anaesthesia and surgery. General and local anaesthetics inhibit in vitro and in vivo important functions of lymphocytes, granulocytes, and macrophages. However, the postoperative immunosuppression is not attributable to the anaesthesia but rather appears to depend on the tissue trauma itself.

Age Factors↗
PubMed1994

Administration of an anti-CD5 immunoconjugate to patients with rheumatoid arthritis: effect on peripheral blood mononuclear cells and in vitro immune function.

OBJECTIVE: An immunoconjugate, CD5 Plus, composed of ricin A chain and murine IgG1 anti-CD5 monoclonal antibody is under investigation for treatment of rheumatoid arthritis. To understand better the mechanism of action of this agent, alterations in immune function and lymphocyte subpopulations were assessed in a subset of patients consecutively enrolled in 2-phase II clinical trials. METHODS: Flow cytometric and in vitro functional analyses of peripheral blood mononuclear cells from 12 patients receiving 5 daily intravenous infusions of CD5 Plus at doses of 0.20 or 0.33 mg/kg were performed before, during and after treatment. RESULTS: Peripheral CD3+ T cells were significantly depleted (p < 0.01) during treatment on Days 2 and 5 and returned towards baseline on Days 15 to 29; changes in CD5+ B cells occurred in parallel. There was no significant treatment effect on monocytes. All T cell subsets examined, including CD4, CD8, CD45RA, CD45RO, HLA-DR+, TCR-alpha beta and TCR-gamma delta, were affected equally through Day 15. On Day 29, the median CD4:CD8 ratio, elevated before treatment, was significantly decreased (p < 0.01), approaching the ratio observed in healthy controls. Proliferative responses to antigenic, allogeneic and mitogenic stimuli in vitro were depressed but detectable during the time of maximal T cell depletion and normalized to baseline values with recovery of T cell number. Spontaneous and pokeweed mitogen induced immunoglobulin secretion were unaffected in these patients. CONCLUSION: Treatment associated effects of CD5 Plus were observed for both T and B cell populations which bear the CD5 antigen, and were reversible, as measured by in vitro assays of immune cell function, phenotype and number.

Adult↗
PubMed1989

Stress reduction training changed number of sexual partners but not immune function in men with HIV.

We tested the impact of stress management training on sexual behavior and immune functioning in 64 gay men infected with human immunodeficiency virus (HIV). Subjects randomized to the stress management group met for eight two-hour sessions and one all day retreat to learn systematic relaxation, health behavior change, and stress management skills. Compared to those randomized to a wait list control, treatment subjects reported significantly fewer sexual partners in the prior month at post-test (1.10 vs 2.29 for controls). There were no differences between groups in lymphocyte numbers and function.

Adult↗
PubMed1978

Iron deficiency, infections, and immune function: a reassessment.

Many physicians believe that patients with iron deficiency have an increased susceptibility to infections. Data in the literature, however, are contradictory, and in many instances the reports are vulnerable to critical review. Literature available through 1976 was analyzed in an attempt to define possible relationships between infections, immune function, and states of iron imbalance, both iron deficiency and overload. Critical points that must be considered for an accurate interpretation were emphasized. It seems clear that the inflammatory response, when assessed by skin reactivity, is diminished in iron deficiency. The precise molecular defect remains undefined, but the abnormality is detected by several assays measuring cell-mediated immunity. Normal function is usually restored following iron repletion.

Anemia, Hypochromic↗
PubMedDate not supplied

Chronic insomnia and immune functioning.

OBJECTIVE: The goal of this study was to investigate whether clinical insomnia is associated with immune alterations by comparing immune functioning between patients with chronic insomnia and good sleepers. METHODS: The good sleepers group was composed of 19 adults with a regular sleep schedule and no complaint of sleep disturbances. The insomnia group was composed of 17 adults meeting criteria for a chronic primary insomnia disorder. Peripheral blood samples were taken at the interview (time 1) and before the second night of polysomnographic assessment (time 2) for immune measures, including enumeration of blood cell counts (ie, white blood cells, monocytes, lymphocytes, and CD3+, CD4+, CD8+, and CD16+/CD56+ cells), natural killer cell activity, and cytokine production (ie, interleukin-1beta, interleukin-2, and interferon gamma). RESULTS: Significant between-group differences were observed for CD3+, CD4+, and CD8+ cells, with higher levels found in good sleepers. In addition, a significant group-by-time interaction was found on monocyte counts. Although this was the only significant interaction effect observed, between-group differences were greater at time 2. CONCLUSIONS: This study suggests that chronic insomnia is associated with some immune alterations. More research is needed to determine the clinical significance of these findings.

Adult↗