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PubMed2001

Nutritional strategies to minimise exercise-induced immunosuppression in athletes.

Strenuous prolonged exertion and heavy training are associated with depressed immune function. Furthermore, improper nutrition can compound the negative influence of heavy exertion on immunocompetence. Dietary deficiencies of protein and specific micronutrients have long been associated with immune dysfunction. An adequate intake of iron, zinc, and vitamins A, E, B6 and B12 is particularly important but excess intakes can also impair immune function. Immune system impairment has also been associated with excess intake of fat. To maintain immune function, athletes should eat a well balanced diet sufficient to meet their energy requirements. An athlete exercising in a carbohydrate-depleted state experiences larger increases in circulating stress hormones and a greater perturbation of several immune function indices. Conversely, consuming carbohydrate during exercise attenuates rises in stress hormones such as cortisol and appears to limit the degree of exercise-induced immunosuppression, at least for non-fatiguing bouts of exercise. Strong evidence that high doses of antioxidant vitamins, glutamine supplementation or echinacea extracts can prevent exercise-induced immunosuppression is lacking.

Dietary Carbohydrates↗

PubMed2003

Neopterin as a new biomarker for the evaluation of occupational exposure to silica.

OBJECTIVES: Silica is one of the most documented workplace contaminants. Long-term occupational exposure to silica is associated with an increased risk for respiratory diseases such as silicosis, tuberculosis, chronic bronchitis, chronic obstructive pulmonary disease and lung cancer. Furthermore, a variety of immune-dysfunction-related diseases has been reported in silicotic individuals. Preliminary studies indicating enhanced levels of autoantibodies and several cytokines reflect an involvement of the immune system in the pathogenesis of silicosis and resulting complications. As an early and valuable biomarker of cellular immunity, neopterin is a low-molecular-mass compound belonging to the class of pteridines. It is produced by guanosine triphosphate via interferon-gamma, following the activation of T cells. The aim of the present study was to observe the alteration of neopterin in silica exposure, and also to show whether screening of neopterin levels may be of use for assessment of occupational exposure to silica. METHODS: In this study, serum and urinary neopterin levels, both in silica-exposed workers ( n=22) and healthy volunteers ( n=20), were investigated by ELISA, spectrophotometry and HPLC techniques. RESULTS: Serum neopterin levels of control and exposed groups were measured as 5.98+ or -0.44 and 7.86+ or -1.97 nmol/l, respectively ( P<0.05). Urinary neopterin levels were also increased in the exposed group: 97.60+ or -41.42 micromol/mol creatinine for controls and 165.59+/-78.20 micromol/mol creatinine for workers ( P<0.05). At the same time, the correlation between urinary neopterin levels, serum neopterin concentration and working years, smoking status, some complaints, and silica status in the working atmosphere were evaluated. CONCLUSIONS: Our findings suggest that the following up of neopterin levels may have diagnostic value in silica-related diseases such as silicosis. Moreover, its biological monitoring should be performed in workplaces for clinical diagnosis and prognosis.

Adult↗

PubMed1992

Gamma-interferon corrects aberrant protein kinase C levels and immunosuppression in the spontaneously hypertensive rat.

The effects of gamma-interferon (gamma-IFN) on protein kinase C (PKC) levels and immunosuppression in the spontaneously hypertensive rat (SHR) were examined. First, an abnormal PKC distribution was found in spleen, thymus and aorta from SHRs relative to normotensive controls. Biweekly injections of rat recombinant gamma-IFN (1000 U/kg) restored basal or resting PKC levels to those found in normotensive Wistar-Kyoto (WKY) rats. We also examined the effects of in vivo gamma-IFN treatment on nuclear PKC (nPKC) activation in purified, isolated splenocyte nuclei. It was found that basal nPKC levels were higher in untreated SHRs than gamma-IFN SHRs or WKYs. Also, while nuclei from untreated SHRs were relatively unresponsive to various immunoreactive substances and PKC activators, gamma-IFN treatment significantly restored activity. Last, the proliferative response to mitogen challenge of isolated splenocytes from untreated SHRs, gamma-IFN-treated SHRs and WKYs was studied. Although gamma-IFN treatment did not restore the proliferative response to that of WKYs, the mitogen response was significantly enhanced by treatment with gamma-IFN. The data show that gamma-IFN acts to restore normal immune function and corrects aberrant PKC levels and adds to the growing body of knowledge suggesting a role for immune dysfunction in the etiology of hypertension.

Animals↗

PubMedDate not supplied

Immune abnormality in relation to nonimmune diseases in SAM mice.

A series of related strains of senescence-accelerated mouse (SAM) shows strain-unique age-related diseases, such as amyloidosis, deficit in learning and memory, osteoporosis, and brain atrophy, while many of these disease-prone mouse (SAMP) strains have impaired immune activity as young adults, and have a short life span, probably not due directly to the diseases. Because the mean life span was prolonged and the time of the disease onset was delayed by a low-calorie dietary condition or a specific pathogen-free environment, both of which ameliorate the impaired immune activity, the enhancement of immune activity may help decrease the deteriorative process of aging, to that seen in ordinary strains of mice. Studies using the SAMP model may help elucidate the role of immunity in the aging process. Herein, we review the cellular and genetic basis of the immune abnormality in SAMP mice, then discuss the relationship between immune abnormality and development of the age-related disease, senile amyloidosis, findings obtained on SAMP hybrid mice and congenic mice for disease-related genes. Activation of the gene(s) for senile amyloid per se shortened the life span, and the early development of the immune dysfunction primarily seems to be both genetically and physiologically independent of amyloidosis, although the disease may be indirectly modified in the aged with depressed immune activity.

Aging↗

PubMed2005

Protein tyrosine phosphatases and the immune response.

Reversible tyrosine phosphorylation of proteins is a key regulatory mechanism for numerous important aspects of eukaryotic physiology and is catalysed by kinases and phosphatases. Together, cells of the immune system express at least half of the 107 protein tyrosine phosphatase (PTP) genes in the human genome, most of which encode multidomain proteins that contain protein- and phospholipid-interaction domains. Here, we discuss the diverse but specific, and important, roles that PTPs have in immune cells, focusing mainly on T and B cells, and we highlight recent evidence that even subtle alterations in PTPs can cause immune dysfunction and human disease.

Animals↗

PubMed2005

Anxiety accelerates T-helper 2-tilted immune responses in patients with atopic dermatitis.

BACKGROUND: Stress, which mediates anxiety, worsens skin symptoms in patients with atopic dermatitis (AD). The contribution of anxiety to immune dysfunction, which plays a critical role in the pathogenesis of AD, requires clarification. OBJECTIVES: To examine the relationship between anxiety and atopy-relevant immune function in AD. METHODS: Eighty-five patients with AD and 58 normal individuals without a history of allergic disorders were enrolled in this study. To assess anxiety, the state-trait anxiety inventory was completed for both groups. In the AD group, measurements were made of SCORAD scores, serum IgE levels, itching (visual analogue scale), blood eosinophil count and T-helper (Th) 1/Th2 ratio in the peripheral blood. RESULTS: Anxiety was significantly higher among the subjects with AD than the normal subjects, and trait anxiety (TA) was higher than state anxiety (SA) in the AD group. Serum total IgE levels were correlated positively with TA and the TA/SA ratio and inversely with SA, and the Th1/Th2 ratio was correlated inversely with TA and the TA/SA ratio. CONCLUSIONS: The patients with AD had higher anxiety levels than normal individuals, and those with a stronger perception of TA than SA showed enhanced serum IgE synthesis and Th2 shifting.

Adolescent↗

PubMed1980

Immunology in dentistry.

Implications of immunology in dental treatment are explained through discussion of the basic scientific principles of allergy, autoimmunity, immunization, immune dysfunction, tumor immunology, immunosuppression, and transplantation immunobiology.

Autoantibodies↗

PubMed2002

Potential for immune reconstitution through G-CSF treatment of HIV patients.

New treatment strategies for HIV/AIDS are very successful in reducing viral load. However, reconstitution of the immune system takes about one year and may be insufficient or remain incomplete. During this time the patient remains prone to opportunistic infections as a result of the complex immune dysfunction caused by the virus. Recombinant granulocyte colony-stimulating factor (G-CSF) has diverse immunomodulatory properties which may be beneficial in aiding immune reconstitution.

AIDS-Related Opportunistic Infections↗

PubMedDate not supplied

Effect of glutamine on immune function in the surgical patient.

The beneficial effects of glutamine on immune function in vitro have been well described. Severely ill surgical patients undergo glutamine depletion and this has been implicated as a cause of immune dysfunction in vivo. With the introduction of the stable dipeptides of glutamine into total parenteral nutrition (TPN) regimens, the clinical effects of glutamine on the immune system have taken on an increased relevance and importance. In a randomized clinical trial, we have shown that glutamine-supplemented TPN increased the T cell mitogenic response in patients undergoing colorectal resection. This was not associated with an altered production of the pro-inflammatory cytokines interleukin-6 (IL-6) or tumor necrosis factor (TNF). In a subsequent clinical trial comparing glutamine-supplemented TPN with control TPN in patients with severe acute pancreatitis there was a similar modest enhancement of the T cell response in the glutamine-supplemented group. Although Il-6 and TNF production were again unchanged, there was a significant reduction in IL-8 production in the glutamine-supplemented group. Glutamine may exert its immunological effects by a direct action on the cells of the immune system. Possible indirect mechanisms by which glutamine may influence the immune system include the maintenance of gut barrier function, or the preservation of action of the antioxidant glutathione.

Glutamine↗

PubMed1999

Changes in immune parameters seen in Gulf War veterans but not in civilians with chronic fatigue syndrome.

The purpose of this study was to evaluate immune function through the assessment of lymphocyte subpopulations (total T cells, major histocompatibility complex [MHC] I- and II-restricted T cells, B cells, NK cells, MHC II-restricted T-cell-derived naive and memory cells, and several MHC I-restricted T-cell activation markers) and the measurement of cytokine gene expression (interleukin 2 [IL-2], IL-4, IL-6, IL-10, IL-12, gamma interferon [IFN-gamma], and tumor necrosis factor alpha [TNF-alpha]) from peripheral blood lymphocytes. Subjects included two groups of patients meeting published case definitions for chronic fatigue syndrome (CFS)-a group of veterans who developed their illness following their return home from participating in the Gulf War and a group of nonveterans who developed the illness sporadically. Case control comparison groups were comprised of healthy Gulf War veterans and nonveterans, respectively. We found no significant difference for any of the immune variables in the nonveteran population. In contrast, veterans with CFS had significantly more total T cells and MHC II+ T cells and a significantly higher percentage of these lymphocyte subpopulations, as well as a significantly lower percentage of NK cells, than the respective controls. In addition, veterans with CFS had significantly higher levels of IL-2, IL-10, IFN-gamma, and TNF-alpha than the controls. These data do not support the hypothesis of immune dysfunction in the genesis of CFS for sporadic cases of CFS but do suggest that service in the Persian Gulf is associated with an altered immune status in veterans who returned with severe fatiguing illness.

Adult↗

PubMed2000

Substance P as prophylaxis for JP-8 jet fuel-induced immunotoxicity.

Previous studies have shown that short-term, low-concentration JP-8 exposure had significant effects on the immune system that persisted for extended periods of time. It was found that administration of aerosolized substance P (SP) was able to protect exposed animals from JP-8-induced immune changes, whereas administration of SP antagonists compounded the deleterious effects ofjet fuel exposure. Thus, SP administration appears to be a relatively simple and efficient means to reverse the immunotoxicity due to hydrocarbon exposure. In the current study, aerosolized SP was analyzed for its potential prophylactic ability to counteract JP-8-induced immunotoxicity. It was observed that concentrations as low as 1 nM were effective in ameliorating the effects of JP-8 exposure on the immune system. SP administered before JP-8 exposure could prophylactically protect both the spleen and thymus from significant organ weight loss, but could not completely restore immune cell numbers to normal, baseline levels. Furthermore, SP treatment could be delayed as long as 1 h postexposure and reverse the effects of jet fuel exposure on immune organ weight loss and immune cell recovery. Significantly, SP could be given 15 min pre-JP-8 exposure but neither 1 nor 6 h pre-JP-8 exposure, and prevent immune dysfunction as measured in mitogenesis assays. However, SP could be delayed up to 6 h post-JP-8 exposure and still almost completely restore immune function. Thus, SP appears able to both prevent and reverse the immunotoxicological effects associated with JP-8 exposure. These results also provide insight into the manner in which JP-8 jet fuel mediates its effects on the immune system.

Animals↗

PubMed1996

Nitric oxide-mediated suppression of T cell responses during Trypanosoma brucei infection: soluble trypanosome products and interferon-gamma are synergistic inducers of nitric oxide synthase.

African trypanosome infections result in lymphocyte unresponsiveness and anemia in the mammalian host. In murine infections, these effects are mediated by suppressor macrophages releasing nitric oxide (NO). We investigated the mechanism of activation of macrophages to produce NO during trypanosomiasis in vitro. A soluble component of trypanosome lysates induced NO synthesis in peritoneal macrophage cultures only when the macrophages were co-stimulated with interferon-gamma (IFN-gamma). The macrophage-activating factor was also released in a soluble form by live bloodstream-form trypanosomes, but not procyclic trypanosomes. When splenocyte cultures were exposed to IFN-gamma and trypanosomes, an NO-dependent suppression of T cell proliferation occurred. This is similar to the suppression observed in the spleens of trypanosome-infected mice, suggesting that a combination of trypanosome-released macrophage-activating factors and IFN-gamma are a trigger of immune dysfunction in trypanosomiasis.

Animals↗

PubMed1999

Murine mercury-induced autoimmunity: a model of chemically related autoimmunity in humans.

Human exposure to certain compounds or therapeutic drugs can result in the development of an autoimmune syndrome. Mercury (Hg) induced autoimmunity is one of the few animal models in which administration of a chemical induces a specific loss of tolerance to self-antigens. After receiving subtoxic doses of Hg or other heavy metals, susceptible mouse strains rapidly develop highly specific antibodies to nucleolar antigens. In addition, these animals display a general activation of the immune system, especially pronounced for the Th2 subset and a transient glomerulonephritis with immunoglobulin deposits. Like many human autoimmune diseases, this syndrome is associated with the expression of susceptible major histocompatibility complex (MHC) class II genes. In this article, we review the essential features of this model, and we discuss the putative mechanisms by which Hg creates such a severe immune dysfunction.

Animals↗

PubMed1997

The expanding role of nerve growth factor: from neurotrophic activity to immunologic diseases.

Numerous studies published in the last 10-15 years have shown that nerve growth factor (NGF), a polypeptide originally discovered in connection with its neurotrophic activity, also acts on cells of the immune system. NGF has been found in various immune organs including the spleen, lymph nodes, and thymus, and cells such as mast cells, eosinophils, and B and T cells. The circulating levels of NGF increase in inflammatory responses, in various autoimmune diseases, in parasitic infections, and in allergic diseases. Stress-related events both in animal models and in man also result in an increase of NGF, suggesting that this molecule is involved in neuroendocrine functions. The rapid release of NGF is part of an alerting signal in response to either psychologically stressful or anxiogenic conditions in response to homeostatic alteration. Thus, the inflammation and stress-induced increase in NGF might alone or in association with other biologic mediators induce the activation of immune cells during immunologic insults. A clearer understanding of the role of NGF in these events may be useful to identify the mechanisms implicated in certain neuroimmune and immune dysfunctions.

Communicable Diseases↗

PubMed1992

Expectation of impaired response to recombinant hepatitis B vaccination.

A controlled trial of hepatitis B vaccination with recombinant antigen was undertaken in 18 hemodialysed end-stage renal failure (ESRD) patients (P) and 16 members of our staff (controls, C). In order to identify expected nonresponders (NR), we monitored T lymphocyte (Tc) subsets, peripheral blood mononuclear cells (PBMC), total leukocytes (WBC) and IgG. After 3 vaccine doses of 40 and 20 IU, respectively, for P and C, at 0, 1 and 6 months, 11 P(61.1%) and all C (100%) responded, as in previous reports [1-3]. The 7 NR presented lower CD4+ Tc fraction, compared to responders (R) and C (p less than 0.05), and higher monocyte (p less than 0.00001) and WBC (p less than 0.002) counts, with lower lymphocyte fraction (p less than 0.001), compared to R. We suggest that NR could represent a selected group of ESRD patients, screenable by these easily detectable features, probably markers of a specific immune dysfunction.

Adult↗

PubMed1999

Paclitaxel enhances macrophage IL-12 production in tumor-bearing hosts through nitric oxide.

Tumor-induced macrophages (Mphis) mediate immunosuppression, in part, through increased production of factors that suppress T cell responsiveness and underproduction of positive regulatory cytokines. Pretreatment of tumor-bearing host (TBH) Mphis with the anticancer agent paclitaxel (Taxol) partially reverses tumor-induced Mphi suppressor activity, suggesting that paclitaxel may restore TBH Mphi production of proimmune factors. Because paclitaxel demonstrates LPS-mimetic capabilities and increased production of the LPS-induced immunostimulatory cytokine IL-12 could account for enhanced T cell responsiveness, we investigated whether paclitaxel induces Mphi IL-12 production. Tumor growth significantly down-regulated Mphi IL-12 p70 production through selective dysregulation of IL-12 p40 expression. LPS stimulation failed to overcome tumor-induced dysregulation of p40 expression. In contrast, paclitaxel significantly enhanced both normal host and TBH Mphi IL-12 p70 production in vitro, although TBH Mphi IL-12 production was lower than that of similarly treated normal host Mphis. Paclitaxel enhanced p40 expression in a dose-dependent manner. Through reconstituted Mphi IL-12 expression, paclitaxel pretreatment relieved tumor-induced Mphi suppression of T cell alloreactivity. Blocking Mphi NO suppressed paclitaxel's ability to induce IL-12 production. This suggests that paclitaxel-induced activities may involve a NO-mediated autocrine induction pathway. Collectively, these data demonstrate that paclitaxel restores IL-12 production in the TBH and ascribe a novel immunotherapeutic component to the pleiotropic activities of NO. Through its capacity to induce IL-12 production, paclitaxel may contribute to the correction of tumor-induced immune dysfunction.

Adjuvants, Immunologic↗

PubMed1981

Single-nutrient effects on immunologic functions. Report of a workshop sponsored by the Department of Food and Nutrition and its nutrition advisory group of the American Medical Association.

Immune system dysfunction can result from singlie-nutrient deficiencies or excesses, alone or in combination with generalized protein-energy malnutriton. Acquired immune dysfunctions in man occur with deficiencies of iron, zinc, vitamins A and B12, pyridoxine, and folic acid and with excesses of essential fatty acids and vitamin E. Additional micronutrients are important for maintaining immunologic competence in animals. Deficits or excesses of many trace elements and single nutrients thus have potential for causing immune dysfunctions in man. Since nutritionally induced immune dysfunction is generally reversible, it is important to recognize and identify clinical illnesses in which immunologic dysfunctions are of nutritional origin. Correction of malnutrition should lead to prompt reversal of acquired immune dysfunctions.

American Medical Association↗

PubMed1989

Dominantly transmitted hematologic dysfunction clinically similar to Fanconi's anemia.

We report a family with a dominantly transmitted syndrome resembling Fanconi's anemia and spanning two generations. This syndrome was characterized by an ill-defined hematologic stem cell disorder, immune dysfunction, poor dentition, hyperpigmented skin, warts, and multiple second trimester spontaneous abortions and included one case of acute myelomonocytic leukemia (acute non-lymphocytic leukemia, M4). This family lacks the characteristic chromosomal aberrations of Fanconi's anemia. We believe this constellation of findings represents an entity not previously described.

Abortion, Habitual↗