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Results for “Immune function”

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At least 307 records · Page 17Linked to original sources
PubMed1990

Suppressive effects of morphine pellet implants on in vivo parameters of immune function.

Chronic morphine treatment elicits a variety of immunosuppressive effects in mice. Most of the work describing this immuno-suppressive activity of the opioid is based on in vitro assessments of the performance of certain components of the immune system in morphine-treated animals. Relatively little has been done by way of tracking the effects of chronic morphine treatment on immunologic parameters in the intact animal. Therefore, this study used several classic in vivo determinations of immune function in mice treated chronically with morphine. Morphine pellet (75 mg) implantation led to a significant inhibition (91%) of paw swelling in a picryl chloride-induced delayed type hypersensitivity response. Uptake of iododeoxyuridine in an in vivo lymphocyte proliferation assay and splenomegaly in a graft vs. host reaction were also significantly suppressed by morphine pellet implantation (34 and 52%, respectively). Coimplantation of a naltrexone pellet (10 mg) completely reversed the suppressive responses to morphine in each assay. Naltrexone alone had no significant effect in any of the assays. The suppressive effects of morphine were less pronounced in adrenalectomized mice in the graft vs. host assay (51% vs. 9% reduction in morphine-pelleted shams relative to morphine-pelleted adrenalectomized mice). These findings indicate the pathophysiologic significance of the previously reported suppression of in vitro correlates of immune function in morphine-pelleted mice. The results further demonstrate that the immunosuppressive effects observed after morphine pellet implantation are naltrexone reversible and suggest that activation of the adrenal is one potential mechanism for this effect.

Animals↗
PubMed1999

Immune function in transgenic mice overexpressing growth hormone (GH) releasing hormone, GH or GH antagonist.

Effects of life-long exposure to high levels of homologous or heterologous growth hormone (GH) and effects of GH resistance on selected parameters of immune function were studied in adult male transgenic mice overexpressing GH releasing hormone (GHRH), bovine (b) GH or an antagonistic bGH analog. In metallothionein I (MT)-bGH transgenic mice with high peripheral levels of bovine GH, there were significant increases in the absolute weight of the thymus and the spleen and in the mitogenic responses of splenocytes to concanavalin A (ConA), lipopolysaccharide (LPS) and phytohemagglutinin (PHA), as compared to age-matched normal animals. There were no significant differences between MT-bGH transgenic and normal mice in splenocyte viability or in delayed-type hypersensitivity measured by the allergic contact dermatitis response to oxazolone. Similar results, including significant stimulation of splenocyte responses to ConA, LPS, and PHA, were obtained in MT-hGHRH transgenic mice in which overexpression of GHRH leads to striking pituitary enlargement and massive elevation of peripheral levels of homologous (mouse) GH. In MT-bGH-antagonist transgenic mice in which overexpression of an antagonistic bGH analog interferes with the actions of endogenous GH, spleen weight was reduced but proliferative responses of splenocytes to ConA, LPS, and PHA were not affected. It is concluded that overexpression of heterologous or homologous GH in transgenic mice can lead to significant stimulation of some parameters of immune function, whereas antagonism of GH action by expression of an antagonistic GH analog does not affect splenocyte responses to mitogens.

Acromegaly↗
PubMed1996

Aging and immune function: a possible role for growth hormone.

Elderly individuals have four to five times the case rate of cancer, tuberculosis and herpes zoster and six to seven times the fatality rate from pneumonia compared to young adults. This may be causally related to two changes that occur with aging, i.e. decreased growth hormone (GH)/insulin-like growth factor-1 (IGF-1) production and decreased immune function. Data from our laboratory as well as others have shown that, based on either GH secretory dynamics or IGF-1 levels, approximately 40% of adults aged 60 and older are GH deficient. In the same population of subjects, immune function decreases such that there is a decline in cell-mediated and humoral immune responsiveness. Some of these immune deficits have been shown to be reversed in humans and primates by GH and/or IGF-1 treatment. This paper will review some of these data.

Adult↗
PubMed1991

Adrenal steroid receptor activation in vivo and immune function.

Recent studies have indicated significant differences among immune and other tissues in in vivo adrenal steroid receptor activation after a given hormone exposure. Nevertheless, the relationship between in vivo receptor activation and functional measures of the immune response has not been determined. Type I and type II adrenal steroid receptor binding in conjunction with mitogen-induced T-cell proliferative responses were measured in the spleens of Sprague-Dawley rats that were administered various concentrations of dexamethasone (DEX). A linear relationship between type II receptor binding and splenocyte proliferation was found, with decreases in measurable type II receptors (indicating in vivo receptor activation) being highly correlated with decreases in immune function. There was no evidence of spare type II receptors. In vitro studies using the type II receptor antagonist RU 486 confirmed that the inhibitory effect of DEX on splenocyte proliferation was mediated via the type II receptor. These findings provide a foundation for future studies evaluating glucocorticoid effects on immune system function and suggest that evidence of in vivo receptor activation may be critical for predicting when and in which tissues adrenal steroid hormones may be capable of modulating the immune response.

Analysis of Variance↗
PubMedDate not supplied

Effects of citrus fragrance on immune function and depressive states.

In our previous experiments on animals evidence was found that citrus fragrance can restore the stress-induced immunosuppression, suggesting that citrus fragrance may have an effect on restoring the homeostatic balance. Since a dysregulation of the neuroendocrine and immune function is thought to be associated with psychosomatic or psychiatric disorders an attempt was made to restore their mental health by stimulation of one of the sensory systems. Fragrance (citrus was our choice) which comforts through stimulation of the olfactory system was applied to depressive patients. It was given to 12 depressive subjects and the results indicated that the doses of antidepressants necessary for the treatment of depression could be markedly reduced. The treatment with citrus fragrance normalized neuroendocrine hormone levels and immune function and was rather more effective than antidepressants.

Adult↗
PubMed1991

Prostaglandins in experimental syphilis: treponemes stimulate adherent spleen cells to secrete prostaglandin E2, and indomethacin upregulates immune functions.

Incubation of microorganisms with macrophages enhances the production of prostaglandin E2 (PGE2). Previous research had indicated that macrophages from syphilitic rabbits suppressed spleen cell synthesis of interleukin-2 (IL-2); this suppressive activity was reversed by indomethacin. Experiments were designed to further characterize the involvement of prostaglandins in immune processing. When Treponema pallidum was incubated with unfractionated spleen preparations, PGE2 production was accelerated, and within 24 h, pharmacologic concentrations of the prostaglandin were detected. When cytochalasin B was used to block phagocytosis, decreased levels of PGE2 were apparent. Commercial preparations of PGE2, in the range generated by macrophage-treponeme interaction, inhibited concanavalin A-induced IL-2 secretion by splenic cells. T. pallidum stimulated IL-1 production by adherent cells, and indomethacin markedly enhanced this effect. In vivo, indomethacin upregulated immune function. Two groups of rabbits were infected, and one was given daily injections of indomethacin for 18 days. Both groups were treated with penicillin to terminate infections. One week later, rabbits were challenged with viable organisms to determine their immune status. The indomethacin-treated group was more resistant to reinfection. In further research, indomethacin enhanced the immunogenicity of vaccine preparations containing heat-killed T. pallidum. Results are discussed in terms of the role of PGE2 as it impinges on immune functions involving macrophage activation (IL-1 production) and T lymphocyte activation (IL-2 production).

Animals↗
PubMed1995

[Effect of low dose rhTNF-alpha on immune function of lymphocytes in burned rats].

SD rats (200-230 g body weight) were randomly divided into three groups: (1) sham burn; (2) burn; (3) burn plus rhTNF-alpha. Third degree burn of 30% TBSA on the trunk was produced in groups 2 and 3. Intravenous rhTNF-alpha(10 micrograms/kg) was administered 6 hours postburn and once daily thereafter for 5 days in group 3. At 5 days postburn, splenic lymphocytes obtained from all the animals were used for the determination of distribution of T lymphocyte subsets with flowcytic analysis and activity of IL-2(Gills method). The results indicated that low dose rhTNF-alpha in vivo could improve distribution of splenic T lymphocyte subsets in burned rats by increasing the numbers of W3/25(Th) and decreasing the number of OX-8(Ts), and the ratio of W3/25/OX-8 was raised. In vitro the proliferation response of T lymphocytes to ConA was enhanced and the activity of IL-2 was increased by 108%, 149% and 168%, respectively, in group 3 compared with that in group 2. However, a dose-dependent effect, in that a small dose (< or = 10 ng/2.5 x 10(6) cells) of rhTNF-alpha improved the immune function of T lymphocytes, while a higher dose inhibited T lymphocyte immune function. These findings showed that rhTNF-alpha improved not only the distribution of T lymphocyte subsets but also their immune activity.

Animals↗
PubMed1998

Severe depression of host immune functions following closed-bone fracture, soft-tissue trauma, and hemorrhagic shock.

OBJECTIVE: To determine the contribution of soft-tissue trauma plus hemorrhage, bone fracture and hemorrhage, as well as the contribution of bone fracture, soft-tissue trauma and hemorrhage on host immune function. SUBJECTS: Adult male mice (n = 6/group). DESIGN: Prospective, randomized, controlled study. SETTING: Animal laboratory at a university-affiliated hospital. INTERVENTIONS: Closed-bone fracture (right lower leg; external fixation) and/or soft-tissue trauma (2.5-cm midline laparotomy, closed in two layers) were induced before hemorrhagic shock (mean arterial blood pressure of 35 +/- 5 (SEM) mm Hg for 90 mins, followed by fluid resuscitation) in male C3H/HeN mice and the animals were killed at 72 hrs after initiation of the experiment. MEASUREMENTS AND MAIN RESULTS: Splenocyte interleukin (IL)-2 and IL-3 release capacity, as well as splenic and peritoneal macrophage IL-1 and IL-6 release capacity were determined. Different traumatic insults, i.e., bone fracture or soft-tissue trauma in conjunction with hemorrhage, produced comparable immune depression. More significant depression of splenocyte IL-2 and IL-3 release capacity as well as macrophage IL-1 and IL-6 release capacity occurred with the combined insult (i.e., bone fracture/soft-tissue injury and hemorrhage) than after bone injury or tissue trauma alone with hemorrhage. CONCLUSIONS: The combination of closed-bone fracture and soft-tissue trauma before hemorrhage leads to even more compromised immunity than either soft-tissue trauma or closed-bone fracture along with hemorrhage. The markedly depressed immune function following bone injury, soft-tissue trauma, and hemorrhagic shock may contribute to the increased susceptibility of severely injured patients to sepsis and the ensuing multiple organ failure in the clinical situation.

Animals↗
PubMed1990

[Effect of plasma from normal individuals and lymphoma patients on immune function].

The effect of plasma from 21 normal donors, 19 patients with non-Hodgkin's lymphoma and 11 patients with systemic lupus erythematosus (SLE) on interleukin 2 (IL-2) responsiveness, T cell proliferation and natural killer (NK) cell activity was studied. IL-2 responsiveness was enhanced by plasma from both normal and patients. The positive rate was 90.4% in normal, 89.5% in lymphoma and 90.9% in SLE, respectively. The same enhancing results were obtained in T cell proliferative assay. In contrast, effect of three kinds of plasma on NK cell activity showed inhibition. The inhibitory positive rate was 52.4% in normal, 36.8% in lymphoma and 81.8% in SLE, respectively. These results indicated that both enhancing and inhibitory effects on different immune functions showed certain specificity. The effect of plasmic substances on various immune responses is beneficial to the investigation of normal and abnormal immunoregulation. Furthermore, it is possible to isolate and purify these immunoregulatory substances as biological regulatory modifiers to modulate the abnormal immune functions.

Cell Division↗
PubMed1975

[Acute leukemia in the terminal phase of Hodgkin's disease: a consequence of the depressed immune function?].

A 52 year old patient suffering from Hodgkin's disease received ionizing radiation and chemotherapy. 7 years after the diagnosis was made he died of acute leukemia. In the recent past similar cases were reported in the literature. There it was suggested that the leukemogenic effect of treatment may be an etiological factor for the development of leukemia. The clinical and experimental data show that the immune function of thymus-dependent lymphocytes is depressed in patients with Hodgkin's disease. According to the Burnet's immune surveillance theory the T-lymphocytes eliminate malignant cells in an early stage. If this T-dependent immune function is depressed - as in Hodgkin's disease - further malignancies may develop.

Acute Disease↗
PubMed1983

Adenosine deaminase deficiency with normal immune function. An acidic enzyme mutation.

In most instances, marked deficiency of the purine catabolic enzyme adenosine deaminase results in lymphopenia and severe combined immunodeficiency disease. Over a 2-yr period, we studied a white male child with markedly deficient erythrocyte and lymphocyte adenosine deaminase activity and normal immune function. We have documented that (a) adenosine deaminase activity and immunoreactive protein are undetectable in erythrocytes, 0.9% of normal in lymphocytes, 4% in cultured lymphoblasts, and 14% in skin fibroblasts; (b) plasma adenosine and deoxyadenosine levels are undetectable and deoxy ATP levels are only slightly elevated in lymphocytes and in erythrocytes; (c) no defect in deoxyadenosine metabolism is present in the proband's cultured lymphoblasts; (d) lymphoblast adenosine deaminase has normal enzyme kinetics, absolute specific activity, S20,w, pH optimum, and heat stability; and (e) the proband's adenosine deaminase exhibits a normal apparent subunit molecular weight but an abnormal isoelectric pH. In contrast to the three other adenosine deaminase-deficient healthy subjects who have been described, the proband is unique in demonstrating an acidic, heat-stable protein mutation of the enzyme that is associated with less than 1% lymphocyte adenosine deaminase activity. Residual adenosine deaminase activity in tissues other than lymphocytes may suffice to metabolize the otherwise lymphotoxic enzyme substrate(s) and account for the preservation of normal immune function.

Adenosine Deaminase↗
PubMedDate not supplied

Impaired immune function in a premature infant with zinc deficiency after total parenteral nutrition.

The report describes a premature infant with necrotizing enterocolitis who developed symptoms of zinc (Zn) deficiency after three to four weeks of total parenteral nutrition (TPN). Clinical presentations included characteristic skin rash, alopecia, retarded growth, generalized edema and decreased serum alkaline phosphatase (ALP). Immune function studies revealed impaired neutrophil adhesion and mitogen-induced lymphoproliferation, whereas phagocytosis, chemotaxis and lymphocyte subsets remained normal. A high dose of elemental Zn (2.5 mg/kg/day), administered orally, improved the clinical symptoms and restored the immune function. In patients with Zn deficiency, impaired neutrophil adhesion and lymphocyte function may contribute to immunodeficiency which can be reversed with adequate Zn supplementation.

Humans↗
PubMedDate not supplied

Immune function in adult highland Papua New Guinea patients with pneumonia.

Immune function and nutritional indices were studied in adult highland Papua New Guinea (PNG) patients with pneumonia, PNG highland controls and expatriate controls living in the Papua New Guinea highlands. Compared to PNG controls, pneumonia patients had higher serum immunoglobulin (Ig)G concentrations, higher salivary IgA:albumin ratios, lower total body weights and a haematological pattern suggesting iron deficiency. PNG controls and pneumonia patients had fewer circulating CD4 and CD8 T lymphocytes than expatriate controls. The proportion of lymphocytes carrying neither T nor B cell markers was higher in PNG subjects than in expatriate controls. These observations indicate that PNG adult pneumonia patients are a distinguishable subpopulation of PNG adults who may be more susceptible than the general population to pneumonia. Decreased circulating T lymphocyte numbers may be, or reflect, a separate risk factor for the entire population.

Adult↗
PubMed1998

Immune function in healthy adolescents.

In the present study, we examine immunological functioning in normal healthy African-American and Latino/Latina adolescents recruited from an inner-city high school and an inner-city clinic. A battery of tests was performed with enumerative and functional measures which encompassed both innate and adaptive immunity. We found immune differences related to age, gender, and race on both the enumerative and the functional immune measures. This data expands the available body of information concerning normal immunity in healthy adolescents.

Adolescent↗
PubMed1984

Influence of nutritional status on immune functions in patients with Crohn's disease.

Nutritional status and immune function were correlated with clinical features in 56 patients with Crohn's disease. These were divided arbitrarily into either undernourished or well nourished groups according to whether their midarm circumference was below or above 90% of ideal standard. Results were also compared with 33 patients with ulcerative colitis and 28 normal subjects. Undernourished patients with Crohn's disease had significantly reduced total lymphocyte and T lymphocyte counts and a reduced proportion of monocytes that ingested latex particles. Well nourished patients with Crohn's disease were similar to the two control groups. Twenty one undernourished patients with Crohn's disease were also followed during the course of two to four months' nutritional treatment with an enteral supplement. Nutritional therapy was associated with significant anthropometric gains as well as significant rises in total lymphocyte and T lymphocyte counts. Serum orosomucoids were significantly higher in undernourished patients and decreased significantly during nutritional therapy. The results show that undernutrition and disease acuity may be associated with reduced immunological competence in patients with Crohn's disease, but all these measurements can be improved by short term nutritional treatment.

Adult↗
PubMed1999

Immune function and phenotype before and after highly active antiretroviral therapy.

Immune functions represented by equal CD4 counts before and after highly active antiretroviral therapy (i.e., pre- and post-HAART) in the same HIV-infected patients, were examined. Twelve HIV-infected patients were included. Patients had equal CD4 counts pre- and post-HAART and were studied on average 30 months pre-HAART and 17 months post-HAART. Post-HAART, CD8+ T cells expressed greater amounts of CD28 (p < .02), smaller amounts of CD38 (p < .02), and a reduced proportion of CD4+CD28+ T cells expressed CD38+ (p < .01). Proliferation increased (p < 10) in lymphocyte cell cultures stimulated with pokeweed mitogens or Candida, and was correlated to expression of CD28 on T cells (p < .02). The proportion of CD3-CD16-CD56+ natural killer (NK) cells increased (p < .05) and CD3-CD16+CD56- NK cells declined (p < .01). Production of interferon-gamma increased (p < .10). The number of naive and memory T cells, the non-major histocompatibility complex (non-MHC)-restricted and HIV-specific MHC-restricted cytotoxicity and the production of macrophage inflammatory protein-1gamma were unchanged. The finding of increased expression of CD28, correlating to increased proliferation capacity, and diminished expression of CD38 on T cells, indicates that following long-term HAART, repopulation occurs with less activated cells with increased proliferative capacity. This finding may be of clinical importance in considering risk and vulnerability for progression of opportunistic infections post-HAART.

Anti-HIV Agents↗
PubMed1998

Glutamine, exercise and immune function. Links and possible mechanisms.

Glutamine is the most abundant free amino acid in human muscle and plasma and is utilised at high rates by rapidly dividing cells, including leucocytes, to provide energy and optimal conditions for nucleotide biosynthesis. As such, it is considered to be essential for proper immune function. During various catabolic states including surgical trauma, infection, starvation and prolonged exercise, glutamine homeostasis is placed under stress. Falls in the plasma glutamine level (normal range 500 to 750 mumol/L after an overnight fast) have been reported following endurance events and prolonged exercise. These levels remain unchanged or temporarily elevated after short term, high intensity exercise. Plasma glutamine has also been reported to fall in patients with untreated diabetes mellitus, in diet-induced metabolic acidosis and in the recovery period following high intensity intermittent exercise. Common factors among all these stress states are rises in the plasma concentrations of cortisol and glucagon and an increased tissue requirement for glutamine for gluconeogenesis. It is suggested that increased gluconeogenesis and associated increases in hepatic, gut and renal glutamine uptake account for the depletion of plasma glutamine in catabolic stress states, including prolonged exercise. The short term effects of exercise on the plasma glutamine level may be cumulative, since heavy training has been shown to result in low plasma glutamine levels (< 500 mumol/L) requiring long periods of recovery. Furthermore, athletes experiencing discomfort from the overtraining syndrome exhibit lower resting levels of plasma glutamine than active healthy controls. Therefore, physical activity directly affects the availability of glutamine to the leucocytes and thus may influence immune function. The utility of plasma glutamine level as a marker of overtraining has recently been highlighted, but a consensus has not yet been reached concerning the best method of determining the level. Since injury, infection, nutritional status and acute exercise can all influence plasma glutamine level, these factors must be controlled and/or taken into consideration if plasma glutamine is to prove a useful marker of impending overtraining.

Animals↗
PubMed1994

Photoperiodic effects on tumor development and immune function.

Seasonal changes in adaptations associated with winter coping strategies have been frequently studied. Central among the suite of energy-saving, winter-coping strategies is the suspension of reproductive activities. The inhibition of reproduction by nontropical rodents is mediated by daylength changes. Although balanced annual energy budgets are critical, survival and subsequent reproductive success also require avoiding predators, illness, and early death. Because the stressors of winter could lead to suppressed immune function, we hypothesized that animals should have evolved survival strategies involving immunoenhancement. Short daylengths provide a predictive cue to individuals that could be used to enhance immune function in advance of stress-induced immunosuppression. In Experiment 1, adult female deer mice (Peromyscus maniculatus) were housed in either long (LD 16:8) or short (LD 8:16) days for 8 weeks, then injected with the chemical carcinogen 9,10-dimethyl-1,2-benzanthracene (DMBA) dissolved in dimethyl sulfoxide (DMSO) or with the DMSO vehicle alone. Animals were evaluated weekly for 8 weeks after injection. None of the animals treated with DMSO developed tumors in any of the experiments. Nearly 90% of the long-day deer mice injected with DMBA developed squamous cell carcinoma. None of the short-day deer mice injected with DMBA developed tumors. Small lesions developed at the site of injection; short-day females had less severe lesions and healed faster than long-day females. Immunoglobulin G (IgG) response to i.p. injection of sheep red blood cells (SRBC) did not differ photoperiodic conditions. The role of estrogens in the photoperiodic responses was evaluated in Experiment 2: Ovariectomized or sham-ovariectomized deer mice received estradiol benzoate replacement therapy or a control procedure in long daylengths for 8 weeks prior to injection of DMBA or DMSO, then were monitored for 8 additional weeks. Females treated with DMBA developed tumors at the same rate, regardless of estrogen manipulation. Estrogen did not affect healing rates. In Experiment 3, female deer mice were injected with a slurry of microspheres that either contained bromocriptine or were empty. Suppression of prolactin with bromocriptine resulted in a decrease of tumor incidence from 55.6% to 24% in long-day females 8 weeks after injection with DMBA. Healing rates were not affected by prolactin manipulations. Silastic capsules that were filled with either melatonin or cholesterol were implanted into long-day female deer mice in Experiment 4; 8 weeks later, females received an injection of either DMBA or DMSO, then were monitored for 8 weeks.(ABSTRACT TRUNCATED AT 400 WORDS)

9,10-Dimethyl-1,2-benzanthracene↗