Micronutrients and immune functions.
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Humans↗
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[Clinical exploration of the immune system by means of the functional immune study].
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Antibodies↗
Alteration of immune function following dietary mycotoxin exposure.
Mycotoxins are a group of structurally diverse fungal secondary metabolites that elicit a wide spectrum of toxicologic effects. Of particular interest is the capacity of some mycotoxins to alter normal immune function when present in foods at levels below observable overt toxicity. Aflatoxin, patulin, citrinin, and zearalenone experimentally alter immunity, and recent evidence suggests that the immunologic effects of ochratoxin A and trichothecenes may have particular significance to human and animal health. For example, the capacity of ochratoxin A to inhibit natural killer cell activity and increase growth of transplantable tumour cells has been associated with renal and hepatic carcinomas in mice and might similarly contribute to human cancer. Impaired resistance to pathogenic microorganisms occurs after exposure to the trichothecenes T-2 toxin and vomitoxin. This may predispose food animals to infectious disease and could result in decreased productivity as well as increased animal-to-human transmission of pathogens such as Salmonella and Listeria. Vomitoxin also alters normal mucosal immune function, specifically at the level of regulation of development, differentiation, and homing of IgA-producing plasma cells. Interestingly, vomitoxin-induced enhancement of IgA production in the systemic compartment contributes to manifestations in the mouse that are highly analogous to human IgA nephropathy, the most common form of human glomerulonephritis worldwide. Over the long term, the extrapolation of mycotoxin-induced immunologic effects observed in inbred mice to actual disease in livestock and humans will require investigations that both simulate natural exposure conditions as well as improve understanding of the cellular and molecular bases for these effects among different species.
Animals↗
Nonsuppression of cortisol in depression and immune function.
Eighteen depressive patients and twenty-five healthy control subjects were studied using a comprehensive immunological test system and the dexamethasone suppression test (DST) as well as some additional neuroendocrine parameters. In addition, immune functions of six of the patients were studied serially three times at 1-2 month's intervals. The OKT 4+/8+ ratio (OKT 4+ = helper/inducer phenotype; OKT 8+ = suppressor/cytotoxic phenotype) was slightly higher in those ten depressive patients showing suppression in the DST than in healthy controls, but there were no significant differences between the nonsuppressor and suppressor groups or between the nonsuppressor and suppressor groups or between nonsuppressors and control subjects. Lymphocyte transformation responses induced by phytohaemagglutinin (PHA) were similar in the nonsuppressors and suppressors, but lower in both groups than in control subjects. The number of Ig-secreting cells measured in the absence and presence of pokeweed mitogen (PWM) were similar in the nonsuppressor and suppressor groups. Four of the depressive patients tested repeatedly exhibited an abnormal response in the DST at the beginning of the study. During the follow-up period two of them recovered completely from depression as well as the patients with a normal suppression in the DST. The proportions of T and B lymphocytes and regulatory T lymphocyte subsets as well as the functions of T and B lymphocytes of the nonsuppressors and suppressors in the DST were within normal ranges before and after recovery from depression and comparable to healthy controls in repeated testing. The results indicate that in spite of the importance of cortisol in immunoregulation, the increased cortisol secretion and typical resistance to dexamethasone suppression in endogenously depressive patients is not profoundly and consistently reflected in immune functions. Neither does normalization of cortisol responses induce any major changes in immune status during a patient's recovery from depression. Previous work indicates that suppressed immunity may play an important role in the increased morbidity and mortality associated with bereavement. In the light of present findings we suggest that endogenous depression differs also in this respect from grief reactions.
Adult↗
[Analysis on the traditional Chinese medicine syndromes of the patients with autoimmune thyroid diseases. Changes in the thyroid and immune functions in 109 cases].
Eighty-nine cases of hyperthyroidism and 20 cases of hypothyroidism caused by Hashimoto's thyroiditis were observed in order to analyse the thyroid and immune functions of the patients, and their relationship with the syndromes of TCM. The results showed that, in the patients with Yin deficiency syndrome, the contents of total T4, T3 were higher than normal and TSH lower than normal, while in Yang deficient patients, the contents of total T4, T3 were lower than normal and TSH higher than normal. This results suggested that the states of thyroid functions were closely related to the TCM syndromes. It was also found that the percentage of OKT 4+ cells and the self-recognizing ability of lymphocytes were lower than normal in patients with hyperthyroidism and Yin deficiency. While in patients with hypothyroidism and Yang deficiency, they were higher than normal. These meant that the abilities of lymphocyte autoreaction in Yin deficient patients were in contrary tendency with those in Yang deficient patients. The former had the manifestation of over-inhibition while the latter, hyperaction. Besides, the contents of auto-antibodies were higher than normal in both the patients with hyperthyroidism and hypothyroidism, which manifested itself as a common character of autoimmune thyroid diseases. The results indicated that there were common characters as well as individual characters of thyroid and immune functions between hyperthyroid patients and hypothyroid patients, and these characters might well be the material bases of various syndromes in TCM.
Adult↗
Modulation of immune function by intestinal neuropeptides.
Direct regulatory control of the immune system by the central nervous system has been postulated. In support of this view is a large body of literature describing immunoregulatory activities of neuropeptides isolated from the gastrointestinal tract. In this review we examine the evidence for expression of specific receptors for gut peptides on immune effector cells and further explore the regulatory effects of these peptides on immune function. Peptides to be discussed include substance P, somatostatin, vasoactive intestinal peptide (VIP), the opioid peptides leu and met enkephalin, calcitonin gene related peptide (CGRP), neuropeptide Y, and cholecystokinin (CCK).
Calcitonin Gene-Related Peptide↗
Progressive multiple sclerosis: abnormal immune functions in vitro and aberrant correlation with enumeration of lymphocyte subpopulations.
In a series of 27 consecutive progressive multiple sclerosis (MS) patients under age 50 we have simultaneously measured 3 in vitro immune functions and 6 markers and compared their results to a group of 21 controls. We have confirmed a reduction of concanavalin A (Con A) -induced suppression and NK function contrasting with increased IgG secretion in response to pokeweed mitogen (PWM). Among 6 monoclonal antibody-recognized subpopulation (Leu 1, Leu 2, OKT8, Leu 3, Leu 7 and Leu 11) only Leu 2+ lymphocytes were statistically reduced. OKT8+ were slightly reduced, Leu 3+ were slightly increased. Discriminant analysis revealed that the 3 immune functions together with the results of OKT8 and Leu 3 enumeration were sufficient to appropriately classify most of the individuals. Only 3 MS and 4 controls were misclassified. Correlation analysis suggested disappearance of the doubly labelled OKT8/Leu 7 population in MS patients. In MS as opposed to controls Con A-induced suppression did not correlate with suppressor cell markers but correlated with NK cell markers suggesting that in MS this population mediates Con A-induced suppression. IgG secretion and Con A suppressor cell function were inversely correlated in MS patients but not in controls, suggesting that in chronic progressive multiple sclerosis a common abnormality underlies both increased response to PWM and decreased induction of suppression by Con A.
Adult↗
Immune function in healthy relatives of patients with malignant disease.
Immune function studies of healthy members of families with multiple lymphoreticular neoplasms were compared with those of healthy members of families with multiple cancers and families with no known history of cancer. The lymphoma family group had a significantly elevated serum level of IgM and diminished responses to the Candida albicans skin test antigen and the T-cell mitogen concanavalin A. Subjects with Epstein-Barr virus-viral capsid antigen titers greater than or equal to 160 had lower responses to mitogens.
Adolescent↗
Immunological abnormalities in rats with adjuvant-induced arthritis--II. Effect of antiarthritic therapy on immune function in relation to disease development.
The effects of the experimental immunomodulatory agent tilomisole (Wy-18,251; (3-(p-chlorophenyl) thiazolo [3,2-a]benzimidazole-2-acetic acid) on disease development and immune function in rats with adjuvant-induced arthritis was assessed in comparison with indomethacin and levamisole. Daily p.o. administration of tilomisole (100-200 mg/kg/day) to M. butyricum-injected rats significantly reduced both edema and bone erosion in the uninjected paw. Moreover, tilomisole treatment restored to normal the diminished Con A-induced proliferative response and IL 2 synthesis observed in spleen cells from arthritic rats, but had no effect on macrophage IL 1 production. In contrast, levamisole treatment (25 mg/kg/day) of arthritic rats improved splenic immune function but did not influence paw edema or bone erosion. Conversely, indomethacin (1 mg/kg/day) significantly reduced paw edema and bone erosion but did not improve the deficient proliferative response or IL 2 synthesis by "arthritic" spleen cells. These results indicate that tilomisole possesses combined antiinflammatory and immunomodulatory activity in adjuvant-arthritic rats which is distinctly different from the effects of either indomethacin or levamisole. Moreover, these data suggest that tilomisole has potential disease-modifying activity in arthritis, which is currently being more closely examined in clinical trials.
Animals↗
Chronic exposure to aldicarb-contaminated groundwater and human immune function.
Aldicarb, a carbamate pesticide, has been a known groundwater contaminant in Wisconsin since 1981. To assess the effects of chronic ingestion of low-level aldicarb-contaminated groundwater (less than 61 ppb) on the immune function of humans, we identified 50 women, ages 18 to 70, with no known underlying reason for immunodysfunction. Twenty-three of these women (exposed group) consumed groundwater with detectable levels of aldicarb, and 27 (unexposed group) consumed water from a source with no detectable levels of aldicarb. Data were collected on each woman's health status, immune function, and fluid intake. Exposed women as compared with unexposed women showed an elevated stimulation assay response to the antigen Candida (P less than 0.02, t test). The exposed group had increased numbers of T8 cells (P less than 0.05, t test), an increased percentage of total lymphocytes as T8 cells (P less than 0.02, t test), and a decreased ratio of T4:T8 cells (P less than 0.02, t test). Our results suggest an association between consumption of aldicarb-contaminated groundwater and abnormalities in T-cell subsets in women with otherwise intact immune systems.
Adolescent↗
Immune function of young adult mice following in utero exposure to cyclophosphamide.
Long-lasting organic damage has been reported following in utero exposure to certain environmental or therapeutic agents. The sensitivity of the developing immune system to chemical insult during organogenesis or histogenesis was evaluated in mice employing the known immunosuppressive agent cyclophosphamide (CY). Experiments were conducted employing one of the following treatment regimens: (1) 1 microgram/g X d intravenously on d 9-12 or 14-17 of gestation; (2) 5 micrograms/g intravenously on 12 of gestation; (3) 1, 2.5, or 5 micrograms/g X d intraperitoneally on d 12 of gestation; or (4) 5, 10, or 20 micrograms/g intraperitoneally on d 17 of gestation. There were no surviving pups born to mothers administered CY by schedule 2; otherwise, numbers of surviving offspring were not affected by drug treatment, and no gross terata were observed. Employing this variety of exposure protocols, consistent enhancement or suppression of cell-mediated or humoral immune function was not observed in offspring of treated dams. Reduced body weight in 5- and 8-wk-old progeny was noted after exposure to 20 micrograms/g on gestational d 17. Increased in vitro B-lymphocyte blastogenic response to lipopolysaccharide occurred in 5-wk-old animals, and production of antibody to sheep erythrocytes was increased in 8-wk-old offspring exposed to CY at 20 micrograms/g on d 17 of gestation. The T-lymphocyte parameters were relatively unaffected by in utero exposure to CY, suggesting either that cell-mediated immune function was not affected by treatment or that homeostasis was restored prior to immunologic evaluation of offspring.
Animals↗
Effects of recombinant bovine interferons-alpha and -gamma on some in vitro immune functions of bovine intraepithelial and lamina propria leukocytes.
The effects of recombinant bacteria-derived bovine interferon-alpha I1 (rBoIFN-alpha I1) and -gamma (rBoIFN-gamma) on some in vitro immune functions of bovine intestinal leukocytes were studied. The proliferative response of intraepithelial leukocytes (IEL) to concanavalin A (Con A) was significantly inhibited by the addition of 5-1,000 U/ml of either IFN type. In contrast, addition of rBoIFN-alpha I1 to lamina propria leukocytes (LPL) from the same animal, showed significant inhibition only above 500 U/ml, whereas rBoIFN-gamma revealed significant enhancement when added as low as 50 U/ml. The concentration of mitogen and the time of incubation were both critical factors in determining the outcome of IFN-leukocyte interactions. While both IFN types could inhibit DNA synthesis of both leukocyte cultures at suboptimal (0.5 microgram/ml) Con A concentration throughout the time of incubation, their modulatory activities varied significantly at optimal (5.0 micrograms/ml) and supraoptimal (50.0 micrograms/ml) Con A concentrations. Preexposure of cells to IFNs or prestimulation with Con A did not significantly change the kinetics of IFNs with both leukocyte cultures. Pretreatment of leukocyte cultures with either IFN type for 18 h significantly enhanced the expression of MHC surface antigens. These data demonstrate that purified IFNs produced by recombinant DNA technology can significantly alter some in vitro immune functions of cells other than circulating leukocytes and that different IFNs have different capabilities to alter leukocyte functions.
Animals↗
Immune function in severe, active rheumatoid arthritis. A relationship between peripheral blood mononuclear cell proliferation to soluble antigens and synovial tissue immunohistologic characteristics.
The immunohistology of synovium from a tender, swollen knee and peripheral blood cellular immune function were correlated in 24 clinically similar patients with active, seropositive rheumatoid arthritis who were not taking cytotoxic or long-acting antirheumatic drugs. The patients were classified as anergic (n = 6) or nonanergic (n = 18) on the basis of peripheral blood mononuclear cell proliferative responses to a battery of soluble recall antigens. The peripheral blood mononuclear cells of anergic patients failed to respond significantly to any soluble recall antigen, whereas cells from nonanergic patients responded to at least one such antigen. Multiple pieces of synovial tissue were obtained from each patient at arthroscopy. To minimize intrajoint variability, all pieces were analyzed and averaged to determine a composite profile of abnormalities. Synovial specimens from all six anergic patients had "high intensity" lymphocytic infiltration (group A). In sharp contrast, synovial specimens from 15 of 18 nonanergic patients had "low intensity" lymphocytic infiltration (group B) (P = 0.002). Group A tissues typically showed higher intensity T cell and plasma cell infiltration, more synovial lining layer hyperplasia, more HLA-DR bearing cells, and a higher ratio of Leu 3A/Leu 2A T cells than did group B. Group B tissues had fewer infiltrating cells (most of which were OKM1 and HLA-DR bearing), more extensive fibrin deposition, and far fewer T and plasma cells. Although these data do not imply that synovium from different joints in an individual patient are immunohistologically identical, they do provide evidence that peripheral blood mononuclear cell immune function reflects immunopathologic events in the biopsied joint. Moreover, the data further support the view that clinically active rheumatoid arthritis is, like certain other chronic inflammatory conditions, a heterogeneous disorder with polar subgroups.
Antigens↗
Reduction of blood pressure and restoration of T-cell immune function in spontaneously hypertensive rats by food restriction and/or by treadmill exercise.
The studies were carried out to compare the effects of food restriction and/or treadmill exercise on the development of high blood pressure and to compare immune function in spontaneously hypertensive rats (SHR). The results demonstrate that moderate food restriction from weaning or a regular treadmill exercise not only maintains significantly lower blood pressure, but also increases T-cell proliferative response against mitogens which is found to be significantly depressed in SHR fed ad libitum. A significant loss of T-cell subpopulation such as W3/25+ T helper cells and OX8+ non-helper T-cells occurring in mice fed ad libitum were restored to normal levels, including IL-2 response, in food-restricted SHR. Our results suggest that both food restriction and/or physical exercise is effective in modulating the blood pressure and increasing T-cell immune functions in SHR.
Animals↗
Reduction of immune function in life stress and depression.
Reduced cell-mediated immune function has been found in depressed patients and in distressed persons undergoing threatening life events. The present study examines the interaction between severe life stress and major depression to produce immune alterations in 36 matched pairs of hospitalized depressed patients and nondepressed controls. Both major depressive disorder and the presence of threatening life events in control subjects are independently associated with a 50% reduction of natural killer (NK) cytotoxicity. A decrease in natural cytotoxicity is significantly associated with depressive symptoms but not with age, alcohol consumption, or tobacco smoking. These findings of altered immunity provide further evidence that the physiological responses in chronic stress parallel those found in the syndrome of depression.
Adult↗
Controlled trial of zinc supplementation during recovery from malnutrition: effects on growth and immune function.
To evaluate the effect of zinc on growth and immune function, 32 marasmic infants were selected on admission to the nutrition recovery center; 16 received 2 mg/kg daily of elemental zinc supplement as acetate and the remaining received a placebo. Immunity was assessed by skin-test response, T-cell blastic proliferation immunoglobulins, and infectious morbidity. Weight-for-length gain for initial 60 days in Zn-supplemented group was 9% of standard vs 3% for placebo (p less than 0.05). Energy intake was similar in both groups. Incidence of infections, especially pyoderma, was significantly higher in placebo group: 10 of 16 vs 3 of 16 in the supplemented group (p less than 0.025). Plasma Zn was correlated with number of febrile days in the prospective month (r = -0.66, p less than 0.05). The percent anergic infants decreased and serum IgA increased significantly only in Zn-supplemented group. Zinc supplementation has significant effects on weight gain and host defense mechanisms despite normal plasma levels. Zinc supplementation is recommended for optimal recovery from marasmus.
Anthropometry↗
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↗
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↗