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PubMed1992

Toxoplasma gondii: an AIDS enhancing cofactor.

Disseminated toxoplasmosis, one of the most severe acquired immune deficiency syndrome (AIDS)-associated infections in humans, is believed to develop from a latent infection after the cellular immune system is suppressed by human immunodeficiency virus type 1 (HIV-1). However, Toxoplasma gondii may serve as a cofactor in enhancing the immunodeficiency induced by HIV-1. This hypothesis is supported by the facts that: 1) co-infection with other pathogens in humans infected with HIV-1 may enhance the progression of the disease to AIDS; and 2) concomitant infection with T. gondii enhances feline immunodeficiency virus-induced immune dysfunction and is likely to cause a more rapid disease onset than an infection with HIV alone. It is possible that T. gondii infection induces tumor necrosis factor (TNF) production. TNF then stimulates the induction of T-cell proteins that bind to the long terminal repeat of HIV-1. This binding at the repeat site then leads to increased HIV-1 activation which causes the dysfunction of CD4 cells and a resulting immunodeficiency that allows even greater amounts of T. gondii replication.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

The acquired immune deficiency syndrome: an overview for the emergency physician, Part 1.

The acquired immune deficiency syndrome (AIDS) was recognized as a distinct entity in 1981. It began as a medical curiosity affecting only several dozen individuals in a restricted segment of the U.S. population. In the 12 years since its description, AIDS has become a pandemic affecting tens of millions with cases reported from all major countries. The illness is caused by a retrovirus, termed human immunodeficiency virus (HIV). It is a blood-borne disease with sexual, parenteral, and perinatal modes of transmission. Infection with the virus can be determined by a number of serologic techniques as well as viral culture. The pathophysiology of illness is incompletely understood, but is in large part related to destruction of helper, CD4 lymphocytes. This results in immune dysfunction and the development of a variety of opportunistic infections and malignancies. A great deal has been learned over the last decade, with important advances in treatment. Zidovudine (AZT) remains the most important agent in slowing progression of the disease and has resulted in prolonging survival. All organ systems can be affected by HIV, and many clinical manifestations are protein. Fever, weight loss, and diarrhea are often encountered general symptoms. The skin is frequently involved, with Kaposi's Sarcoma the most common malignancy and a variety of fungi and viruses the most frequent cause of infection. The lung is involved in the majority of patients, with Pneumocystis Carinii (PCP) and mycobacteria emerging as the most important pathogens. A variety of treatments have demonstrated efficacy for PCP. The risk of PCP is related to the decay in CD4 lymphocytes so that prophylactic treatment is recommended when CD4 counts fall below 200. Mycobacterial infection with multiresistant organisms has complicated the management of these infections and poses new risks to health care workers. Part 1 of this two-part series on AIDS discusses the pathophysiology and clinical expression, epidemiology, laboratory testing, and the general clinical manifestations of AIDS, as well as dermatologic, pulmonary, and cardiac symptoms. Part 2 will discuss the gastrointestinal, neurologic, and ocular symptoms, as well as the treatment and management of the AIDS patient.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Alcohol stimulation of lipid peroxidation and esophageal tumor growth in mice immunocompromised by retrovirus infection.

Tumor appearance can be accelerated in the immunodeficient and immunosuppressed animal. The role of lipid peroxidation and immune dysfunction induced by retrovirus and ethanol treatments on cancer promotion were investigated. Following the initiation of esophageal cancer by methylbenzylnitrosamine, ethanol consumption and retrovirus infection individually and concomitantly increased growth of esophageal tumors. Dietary supplementation with vitamin E reduced the size and frequency of the developed tumors. Tumor growth modifications in the vitamin E supplemented animals may be due to changes in T-cell numbers and functions stimulated by vitamin E. In addition, increased production of free radicals following ethanol treatment and retrovirus infection, and the suppression of these formations lipid peroxide by vitamin E is accompanied by lower incidence and size of tumors. Thus, the mechanisms of tumor enhancement observed in immunocompromised animals may include a combination of immunomodulation and modification of oxidant production by ethanol consumption and retrovirus infection.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Autoimmune insulin syndrome.

Initially described in Japan, the autoimmune insulin syndrome is caused by the presence of anti-insulin antibodies in patients who have never received insulin. This syndrome accounts for spontaneous or reactive hypoglycaemia with very high levels of total immuno-reactive insulin. Discordance between the levels of immunoreactive insulin and C peptide indicate the possible presence of anti-insulin antibodies; this can avoid an incorrect diagnosis of insulinoma. These autoimmune hypoglycaemias often present a difficult diagnostic problem in distinguishing them from factitious hypoglycaemia. The course of the autoimmune insulin syndrome is usually favourable, with a spontaneous rapid diminution of the levels of anti-insulin antibodies. The reasons for the appearance of anti-insulin antibodies and the exact mechanisms of the hypoglycaemia remain uncertain. However, the frequent association of the autoimmune insulin syndrome with certain autoimmune diseases suggest a common immune dysfunction. Drugs containing a sulphydryl group have been implicated in the aetiology of this syndrome.

Autoimmune Diseases↗
PubMedDate not supplied

Schizophrenic births and viral diseases in two states.

In order to investigate a possible relationship between schizophrenic births and viral diseases, the birth month and year of all state hospital admissions for schizophrenia in Connecticut and Massachusetts from 1973-1974 were compared with the occurrence of reportable viral diseases for 1920-1955. Data was statistically examined by time series using spectral analysis. Statistically significant coherences were found between schizophrenic births and measles (both states), varicella-zoster (Connecticut) and polio (Connecticut). Influenza just missed statistical significance. No temporal relationship between schizophrenic births and rubella or mumps was found. The results are compared with similar studies in Minnesota and Finland. Definitive explanations for the observed relationships are precluded by the emerging complexity of virus-CNS interactions. A triggering of immune dysfunction by the infectious agents is proposed as the most reasonable explanation.

Connecticut↗
PubMed2005

Corticotropin-releasing factor-binding protein, stress and major depression.

Major depressive disorder (MDD) is characterized by a dysregulation of the stress response system. A corticotropin-releasing factor (CRF) hyperdrive is a consistent and well-documented finding. CRF-binding protein (CRF-BP) may play a role in the pathogenesis of MDD. CRF-BP reduces the availability of CRF by binding free CRF and inhibits CRF function at the pituitary level. Moreover, CRF-BP expression increases in the pituitary and amygdala in response to acute stress, providing an additional feedback mechanism to maintain the homeostasis of the stress response. There are different regulatory elements of the expression of CRF-BP gene that are implicated in the pathophysiology of MDD, including CRF, glucocorticoids, cytokines and estrogens. A specific haplotype within the CRF-BP gene has been associated with MDD, but confirmation of this finding is necessary. Currently, the possible role of CRF-BP in the pathophysiology of conditions that have been associated with a hypofunction of the CRF system and immune dysfunctions is unclear. Implications of the function of CRF-BP for therapeutic strategies in MDD are being discussed. An important advantage of ligands that target CRF-BP is that concentrations of free CRF can be altered without acting directly on the transmission of CRF through its receptor.

Aging↗
PubMed2004

Alterations in mast cell function and survival following in vitro infection with human immunodeficiency viruses-1 through CXCR4.

HIV-1 infection leads to a disease that attacks the central regulatory mechanisms of the immune response. As mucosal tissue is one of the primary sites infected with HIV in vivo, we examined the effects of HIV exposure on human mast cells, important components of mucosal defense. Using the human mast cell line, HMC-1, which expresses CXCR4 but not CCR5 on the cell surface, we found that several HIV-1 X4 tropic lab (IIIB, RF) and primary isolates but not R5 (BAL, ADA) isolates productively infected these cells. Furthermore, stem cell factor-dependent mast cells derived from primary fetal liver or cord blood cultures were also productively infected with both X4 and R5 HIV-1 strains. Infection was blocked at the level of viral entry using monoclonal antibodies to CXCR4 and CD4. Treatment of HMC-1 with TNF-alpha and TGF-beta stimulated cell surface expression of CCR5 and up-regulated expression of both CCR5 and CXCR4 on primary mast cells, leading to increased susceptibility to both X4 and R5 viral isolates. HIV-1 infection also resulted in histamine release from these mast cells, most due in part to HIV-mediated cell death. These results demonstrate that X4 viruses can use CD4 and the CXCR4 receptor to infect mast cells, suggesting that mast cell-T cell interactions may contribute to HIV mediated immune dysfunction in the mucosa.

Apoptosis↗
PubMed2004

Iron chelators increase the resistance of Ataxia telangeictasia cells to oxidative stress.

Ataxia telangeictasia (A-T) is an autosomal recessive disorder characterized by immune dysfunction, genomic instability, chronic oxidative damage, and increased cancer incidence. Previously, desferal was found to increase the resistance of A-T, but not normal cells to exogenous oxidative stress in the colony forming-efficiency assay, suggesting that iron metabolism is dysregulated in A-T. Since desferal both chelates iron and modulates gene expression, we tested the effects of apoferritin and the iron chelating flavonoid quercetin on A-T cell colony-forming ability. We demonstrate that apoferritin and quercetin increase the ability of A-T cells to form colonies. We also show that labile iron levels are significantly elevated in Atm-deficient mouse sera compared to syngeniec wild type mice. Our findings support a role for labile iron acting as a Fenton catalyst in A-T, contributing to the chronic oxidative stress seen in this disease. Our findings further suggest that iron chelators might promote the survival of A-T cells and hence, individuals with A-T.

Animals↗
PubMed2005

Genetic aspects of pulmonary responses to inhaled pollutants.

Air pollution continues to be a major public health concern in industrialized cities throughout the world. Recent population and epidemiological studies that have associated ozone and particulate exposures with morbidity and mortality outcomes underscore the important detrimental effects of these pollutants on the lung. Inter-individual variation in human responses to air pollutants suggests that some subpopulations are at increased risk to the detrimental effects of pollutant exposure, and it has become clear that genetic background is an important susceptibility factor. Environmental exposures to inhaled pollutants and genetic factors associated with disease risk likely interact in a complex fashion that varies from one population to another. The relationships between the genetic background and disease risk and severity is often evaluated through traditional family-based linkage studies and positional cloning techniques. Case-control studies based on association of disease or disease subphenotypes with candidate genes may have certain advantages over family pedigree studies, and have become useful for understanding complex disease phenotypes. This is based in part on continued development of quantitative analysis and development of mapping technologies. Linkage analyses with genetically standardized animal models are useful to identify genetic determinants of host responses to environmental stimuli. For example, linkage analyses using inbred mice have identified chromosomal segments (quantitative trait loci, QTL) that contain genes that control susceptibility to the lung inflammatory and immune dysfunction responses to ozone, nitrogen dioxide, zinc oxide, and sulfate-associated particles. Candidate genes within the pollutant susceptibility QTLs have been tested for proof-of-concept using gene-targeting and overexpression models. Importantly, significant homology exists between the human and mouse genomes. Therefore, comparative mapping between the human and mouse genomes should yield candidate susceptibility genes that may be tested by association studies in humans. The combined human studies and mouse modeling will provide important insight to understanding genetic factors that contribute to differential susceptibility to pollutants in human populations.

Air Pollutants↗
PubMed2005

Mycobacteria in drinking water distribution systems: ecology and significance for human health.

In contrast to the notorious pathogens Mycobacterium tuberculosis and M. leprae, the majority of the mycobacterial species described to date are generally not considered as obligate human pathogens. The natural reservoirs of these non-primary pathogenic mycobacteria include aquatic and terrestrial environments. Under certain circumstances, e.g., skin lesions, pulmonary or immune dysfunctions and chronic diseases, these environmental mycobacteria (EM) may cause disease. EM such as M. avium, M. kansasii, and M. xenopi have frequently been isolated from drinking water and hospital water distribution systems. Biofilm formation, amoeba-associated lifestyle, and resistance to chlorine have been recognized as important factors that contribute to the survival, colonization and persistence of EM in water distribution systems. Although the presence of EM in tap water has been linked to nosocomial infections and pseudo-infections, it remains unclear if these EM provide a health risk for immunocompromised people, in particular AIDS patients. In this regard, control strategies based on maintenance of an effective disinfectant residual and low concentration of nutrients have been proposed to keep EM numbers to a minimum in water distribution systems.

Amoeba↗
PubMed2006

Effects of silymarin on the proliferation and glutathione levels of peripheral blood mononuclear cells from beta-thalassemia major patients.

Iron toxicity in beta-thalassemia major is the main cause of oxidative stress and cell mediated immune deficiencies. Despite indicative signs of severe oxidative deficiencies associated with beta-thalassemia major, such as decreased level of plasma antioxidants and depletion of erythrocyte glutathione, little is known about intracellular redox status of immune cells. Since glutathione is a primary intracellular antioxidant and plays an essential role in several functions in T cells, in this study intracellular glutathione (GSH) levels as well as proliferation of PHA-activated peripheral blood mononuclear cells (PBMC) were investigated in 28 beta-thalassemia major patients and 28 healthy age-matched individuals. Considering the potential benefits of flavonoids in the therapy of oxidative stress, the effects of silymarin on the GSH levels and proliferation of PBMC from normal and thalassemia individuals were further examined. Quantitative determination of intracellular GSH and proliferative response of PBMC to PHA were performed before and after 72 h incubation of PBMC with various concentrations of silymarin (0, 5, 10, or 20 mug/ml). Results demonstrated a significant reduction of GSH and proliferation in beta-thalassemia major cells; however treatment with silymarin led to restoration of both GSH levels and PBMC proliferation in thalassemia patients. Considerably low levels of GSH and depressed proliferative response of PBMC in beta-thalassemia major may be responsible for the cell mediated immune abnormalities in iron overload conditions. Moreover, the GSH restoration and improvement of PBMC growth by silymarin is a possible explanation for its recently reported antioxidant and immunostimulatory activities. These data suggest the benefit of using flavonoids to normalize immune dysfunction in beta-thalassemia major. The immunomodulatory effects of silymarin in beta-thalassemia major are currently under further investigation in a double blind clinical trial.

Adolescent↗
PubMed2004

Novel concepts and treatments for autoimmune disease: ten focal points.

Understanding the development of autoimmunity is a crucial step toward improving the management, not only of autoimmune diseases, but also of tumors and primary immunodeficiency syndromes. The rapid expansion of knowledge on autoimmunity is fueling the development of a novel approach known as targeted immunotherapy. The present review will concentrate on ten areas where major advances have been achieved: 1) early regulation of B-cell mediated autoimmunity; 2) thymic regulation of tolerance to tissue-restricted antigens via the transcription factor AIRE; 3) role for a population of regulatory T cells (CD4+ CD25+ Tregs) with unique effects; 4) major role for dendritic cells in the development of autoimmunity in conditions such as lupus; 5) role for T cells in autoimmune diseases; 6) role for T cells in rheumatoid arthritis, with new data from a murine model of spontaneous arthritis related to a ZAP-70 mutation; 7) role for the environment via innate immunity, in particular mediated by the toll-like receptors (TLR); identification of new autoantigens with the description of sense-antisense peptides (e.g., proteinase 3-complementary proteinase 3); the immunosenescence concept, which suggests that some autoimmune diseases may be related to premature aging of the immune system; 10) identification of new immunotherapy targets, including costimulation pathway molecules (CD28, CTLA4), original activation systems (BAFF/BLyS), and receptors such as TLRs. These exciting insights into the pathogenic mechanisms underlying immune dysfunction will play a key role in advancing the field of immunorheumatology.

Autoimmune Diseases↗
PubMed2005

Bone and joint disease associated with primary immune deficiencies.

Primary immune deficiencies (PIDs) are characterized by functional and/or quantitative abnormalities of one or more immune system components. Several bone and joint abnormalities can occur in patients with PID, with arthritis being the most common. Joint manifestations, of which arthritis is the most common, occur chiefly in humoral PIDs (agammaglobulinemia, common variable immunodeficiency, hyper-IgM syndromes, and IgA deficiency) and occasionally in other PIDs (chronic granulomatous disease and Wiskott-Aldrich syndrome). Monoarthritis or oligoarthritis is the usual pattern, although polyarthritis may occur, occasionally with nodules suggesting rheumatoid arthritis. Arthritis in patients with PID is usually infectious in nature, the most common causative organism being Mycoplasma, followed by Staphylococcus, Streptococcus, and Haemophilus. These bacteria can induce not only synovial infections, but also aseptic arthritogenic inflammatory responses. Arthritis having no demonstrable relation to chronic infection has been reported also and ascribed to dysimmunity-driven mechanisms that exhibit a number of specific features. Bone lesions are far less common and usually due to infections complicating humoral PID. Distinctive bone manifestations occur in a number of rare PIDs (e.g., hyper-IgE syndrome and Di George syndrome) and in syndromes characterized by spondyloepiphyseal dysplasia. Familiarity with PID syndromes both enhances the diagnostic capabilities of physicians and provides insight into the pathophysiology of bone and joint abnormalities associated with immune dysfunction. In children and occasionally in adults, a combination of bone and/or joint manifestations and hypogammaglobulinemia may indicate PID. When there is no evidence of lymphoproliferative disease, infection, or iatrogenic complications, investigations for PID should be obtained. PID-related arthritis is a unique model for studying the pathogenesis of presumably postinfectious arthritis and of inflammatory joint diseases including rheumatoid arthritis.

Agammaglobulinemia↗
PubMed2004

Chemokine networks and in vivo T-lymphocyte trafficking in nonhuman primates.

T-lymphocyte migratory circuits in human and nonhuman primates remain largely unexplored due to the difficulty of defining cell trafficking in vivo. However, this knowledge may reveal critical aspects of immunity and T-lymphocyte homeostasis in both health and disease. Furthermore, in vivo T-lymphocyte trafficking studies may facilitate defining mechanism(s) of immune dysfunction in the nonhuman primate model for acquired immunodeficiency syndrome (AIDS). Here, we developed a model for in vivo T-lymphocyte trafficking in nonhuman primates, and delineated homing characteristics of unstimulated peripheral blood mononuclear cells (PBMCs) to lymphoid and nonlymphoid compartments in healthy rhesus macaques. T-lymphocyte homing of autologous, carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled PBMCs was defined within 48 h of intravenous transfer. The highest relative frequency of CFSE+ T lymphocytes was observed in peripheral blood and spleen. Expression of chemokine receptor CCR7 and its ligands correlated with recirculation of T lymphocytes through the periphery and homing to paracortical regions of lymph node, where cells remained largely excluded from B-cell follicles. T-lymphocyte trafficking was also detected to the liver and bone marrow, and at low levels to the thymus and small intestine. The liver contained the highest proportion of CD45RA- T lymphocytes, consistent with homing of activated/memory T lymphocytes to this nonlymphoid site. Our data suggest that lymphoid and nonlymphoid organs are under continuous immunosurveillance in healthy macaques, and that this model may serve to investigate aberrant patterns in disease.

Animals↗
PubMed2006

B7-H3 and B7-H4 expression in non-small-cell lung cancer.

Inhibitory regulatory functions of B7-H3 and B7-H4 regarding T-cell activation have been reported recently. Little is known about the significance of human B7-H3 and B7-H4 expression in non-small-cell lung cancer (NSCLC), and we conducted the present study to address this issue in cell lines and tumor tissue from 70 patients. B7-H3 is over-expressed by all six NSCLC cell lines on both mRNA and protein level. B7-H4 is only transcripted by one cell line in which an alternatively spliced form was discovered. In tumor tissues, expression of B7-H3 and B7-H4 was found both on the cell membrane and in the cytoplasm. Thirty-seven percent of the specimens expressed B7-H3 and 43% B7-H4. The number of T infiltrating lymphoid cells (TILs) in the tumor tissues that expressed B7-H3 or B7-H4 was much lower than those who did not. There was a significant positive relation between the expression of B7-H3 and B7-H4, and high B7-H3 or B7-H4 expression was significantly more common in cases with lymph node metastasis. These observations suggest the contribution of B7-H3 and B7-H4 to immune dysfunction and tumor progression in NSCLC patients. B7-H3 and B7-H4 may be an important target for diagnosis and/or therapy of NSCLC.

Adenocarcinoma↗
PubMed2004

The immunoregulatory effects of homocysteine and its intermediates on T-lymphocyte function.

Elevated levels of homocysteine (Hcy) have been identified as independent risk identifiers for cardiovascular disease, cerebrovascular disease as well as for all-cause mortality. Despite the potential importance of these observations, a definitive pathological role for Hcy or its various metabolites in any of these conditions has not been established. Particularly deficient is a description of the effects of elevated levels of homocysteine on immune function. Folic acid and vitamin B12 deficiency have been independently associated with decreased immune function, the apoptosis of bone marrow hematopoietic progenitor cells and the appearance of leukocytes with hypomethylated DNA in the peripheral circulation. A specific role for Hcy or its metabolites in these processes has not been described. We have examined the effects of Hcy and its various derivatives on T cell activation, differentiation and cell viability. Our results have demonstrated that Hcy is a potent concentration-dependent T cell activator promoting cellular activation and differentiation as well as potentiating activation-induced cell death (AICD) and cellular apoptosis. Overall, Hcy appears to exert diverse effects on immune function in the circulation and within the tissue microenvironment possibly contributing to age-related immune dysfunction and disease pathology.

Aged↗
PubMed2004

Role of melatonin in carbon monoxide-induced hypoxemia.

Melatonin (MEL) works in tandem with serotonin (5HT), where an equilibrium exists in perfect health. Under stress or in crisis, it may be that the production of MEL predominates in conjunction with ever increasing production of reactive oxygen species (ROS), may lead to hypoxemia and consequently, to metabolic disruption. The Melatonin Hypothesis could offer an explanation towards certain clinical observation and may support the Catacholamine Hypothesis in the development of depression but it is the role played by carbon monoxide (CO) in inducing hypoxemia which may result in the Cascade Effect that could in turn explain the development of neurodegenerative, neurodevelopmental as well as immune dysfunctional type disorders, prevalent today. CO-induced hypoxemia is an important aspect in any discussion of cell integrity as CO is formed endogenously from the degradation of erythrocytic heme, any hemolytic disturbance or lipid peroxidation, may increase the level in blood. CO, in inducing hypoxemia, causes the generation of large quantities of hydroxyl (-OH) which could damage specific amino acid and disorder protein metabolism that may result in the creation of toxic metabolites. Hydroxyl damage is emerging as the precursor to low-grade inflammation in the presence of C Reactive Protein (CRP) that is currently speculated in the etiology of many known disorders. As disordered protein metabolism may play a crucial role in the formation of the cascade, the hypothesis aims to address the issues of cell viability and the process of cell replication in the event where cell integrity is severely compromised in the face of apoptotic and/or necrotic damage, as the intra-cellular and extra-cellular environments are becoming increasingly hostile. Where -OH damage to specific amino acid in protein may contribute to the Cascade Effect, the hypothesis goes further to explain the importance of the Circardian Cycle and the role of paradoxical sleep, by taking into consideration the need for repair and for regeneration in order to maintain morphology as any cellular event that depends on a redox state is likely to be compromised in an event of hypoxemia. As MEL enters a cell readily because of its high lipid solubility, the role of MEL becomes clear as in its diversity, MEL is a potent oxygen radical scavenger that operates throughout the cell.

Carbon Monoxide↗
PubMed2005

Interferon-gamma- and interleukin-4-producing T cells in Down's syndrome.

Down's syndrome (DS) associates with genetic-dependent dysregulation of the interferon (IFN) system. We used intracellular cytokine staining to analyse the percentages of IFN-gamma- and interleukin (IL)-4-producing T cells in the peripheral blood of patients with DS, individuals with mental retardation (MR), and healthy controls (HCs). The percentages of IFN-gamma-producing CD4(+) and CD8(+) T cells (IFGCs), namely Th1 (mean, 21.4+/-S.D. 1.3) and Tc1 (12.6+/-1.1), and the Th1/Th2 ratio (6.1+/-0.2) in DS were significantly higher than in MR (15.9+/-1.3, 7.9+/-0.6, 4.8+/-0.3) and in HCs (15.6+/-1.9, 7.2+/-1.1, 4.6+/-0.6). Most of the DS patients with high IFGC percentages were seropositive for anti-transglutaminase IgA. We found no correlation between sex, age, APOE genotypes, coexisting autoimmune diseases, susceptibility to infections, or degree of cognitive impairment and high IFGC percentages. This abnormality might thus contribute to immune dysfunction in DS without manifest clinical correlates.

Adult↗