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At least 1,801 records · Page 100Linked to original sources
PubMed2005

The search for a tuberculosis vaccine: an elusive quest?

The precise mechanisms of protective immunity and pathogenesis of tuberculosis (TB) are poorly understood. Yet, many efforts are underway to develop new, more effective vaccines against Mycobacterium tuberculosis. This development appears to be predicated upon the assumption that natural acquired immunity to TB exists. In this paper we review the evidence for such immunity, explore the hypothesis that disease progression is due to some, often transient, immunological dysfunction, and discuss its relevance for vaccine development. Several mechanisms for such an immune dysfunction are proposed, including the recently suggested involvement of viral co-infections. Developing vaccines for such co-infections may be a new challenge for TB control.

Communicable Disease Control↗
PubMed1985

Experimental model for the otitis media with effusion induced by Arthus' reaction.

The Arthus' reaction in the middle ear cavity was studied using histochemical technique. The deposition of immune complex on the basement membrane and the immune complex in the middle ear effusion were the initial features of these animal models. But, these immune complexes were clearly removed from the tympanic cavity during the early phase of reaction. Immune complexes were supposed to be just a initiation of otitis media with effusion. The tubal dysfunction and local immunity of middle ear mucosa caused by the Arthus' reaction seemed to be responsible for the chronicity and relapsing of otitis media with effusion respectively.

Animals↗
PubMed2006

Pathogenesis of idiopathic inflammatory myopathies.

The idiopathic inflammatory myopathies, myositis, are characterized by a chronic course with decreased muscle endurance and by infiltrates of T lymphocytes and macrophages in muscle tissue. Treatment with immunosuppressives rarely leads to recovery of muscle function, despite abolishment of inflammatory cell infiltrates in muscle tissue. Therefore, other mechanisms than immune-mediated muscle fiber damage are likely to contribute to the pathogenesis. One such non-immune-mediated muscle dysfunction could be caused by a disturbed microcirculation due to capillary loss or to phenotypically changed endothelial cells in the capillaries. These aberrations may affect the micro-environment of muscle tissue and lead to local tissue hypoxia with development of a secondary metabolic myopathy. Another possible non-immune-mediated mechanism leading to muscle dysfunction is the newly identified endoplasmatic reticulum (ER) stress response in myositis. The ER stress response is thought to be a consequence of the up-regulation of major histocompatibility complex class I in muscle fibers. These newly identified molecular pathways could play a major role in the pathogenesis of myositis and could be important targets in the development of new therapies.

Humans↗
PubMed2000

Metabolic, neuroendocrine and immune functions in basal conditions and during the acute-phase response to endotoxic shock in undernourished rats.

Chronic malnutrition is one of the most important causes of several metabolic, immune and neuroendocrine dysfunctions. The aim of the present study was to determine the influence of chronic food restriction on basal neuroendocrine, immune and adipocyte functions and during the acute-phase response to endotoxic shock in female rats. The effect of refeeding of undernourished rats on the above-mentioned functions was also investigated. For these purposes, plasma total protein, glucose, triglycerides, ACTH, corticosterone, tumor necrosis factor-alpha (TNF) and leptin (LEP) levels were determined in basal condition and 2 h after endotoxin (LPS; 180 microgram/kg body weight, i.p.) administration in 3 different groups: (1) well-nourished (WN) controls; (2) undernourished (UN) rats as a consequence of chronic food restriction, and (3) UN rats re-fed to restoration of their body weights in the WN rat range. The results indicate that UN rats, in comparison with WN controls, developed an arrest in body weight gain as well as in basal hypoglycemia, hypotriglyceridemia, hypoleptinemia, hypercorticosteronemia and enhanced adrenal glucocorticoid content; however, no changes in basal total protein, ACTH and TNF plasma levels and in anterior pituitary ACTH concentrations were found. When endotoxic shock was induced, the LPS-induced hypoglycemia developed in WN rats was abolished in UN animals, and both ACTH and TNF plasma concentrations after endotoxin, albeit significantly (p < 0.05) higher than the respective basal values, were significantly (p < 0.05) lower in UN than in WN control rats. Despite the high basal plasma corticosterone concentration in UN vs. WN rats, the LPS-induced glucocorticoid release was similar in WN and UN rats. Additionally, LPS treatment did not modify basal plasma LEP levels, regardless of the group. Interestingly, UN rats fed ad libitum for 15 days restored their body weight to WN rat range values, and the various metabolic dysfunctions seen in UN rats in both basal and post-LPS conditions were fully normalized. Our results clearly indicate that chronic undernutrition not only affects, as earlier described, reproductive function but also metabolic, neuroendocrine, immune and adipocyte functions, and that the effects induced by undernutrition can be fully reversed after recovery of normal body weight. The present study strongly supports the involvement of the metabolic status in the effectiveness of the defense mechanisms developed in patients in inflammatory stress conditions.

Acute-Phase Reaction↗
PubMed1994

Exercise and immunology.

The documented effects of physical activity on host defense date to the early 1900s, although the influences of exercise on infectious and neoplastic disease susceptibility in healthy persons have long been subject to widespread disagreement. Even less is known of the effects of exercise in reducing illness predilection for persons already susceptible to, or afflicted by, immune disease or dysfunction. Recently, however, reports suggest that exercise may reduce the incidence and severity of infection. These reports have been bolstered by well-conducted epidemiologic and laboratory studies demonstrating a link between moderate exercise and either heightened immune function or reduced disease incidence, a relationship that is reversed in instances of immoderate exercise. This symposium will present current information addressing beneficial and detrimental influences of exercise on immune function and disease susceptibility. The authors will emphasize direct effects of acute exercise and physical training on immune cells and their neuroendocrine/immune modulators. The relationship among exercise, infection susceptibility, and immune system function will be highlighted, as well as exercise-induced activation of, and illness/disease regulation by, natural killer cells. Consequences of exercise on immune function and disease advancement will be addressed for persons with neoplasia, autonomic dysfunction, aging-related immunosenescence, and AIDS.

Disease Susceptibility↗
PubMed1997

Inflammatory cell-derived NO modulates cardiac allograft contractile and electrophysiological function.

We previously demonstrated that inhibition of inducible nitric oxide (NO) synthase (iNOS) ameliorated acute cardiac allograft rejection. This study used a rat cardiac transplant model to characterize contractile and electrophysiological dysfunction during early acute rejection, further examine the role of NO and iNOS in this process, and determine which cells expressed iNOS during early rejection. During early acute rejection, before significant myocyte necrosis, allograft papillary muscles had reduced tension development and rates of tension development and decline during beta-adrenergic, adenylate cyclase, and calcium stimulation compared with isograft and normals [e.g., tension of 36 (allograft) vs. 73 (isograft) mN/mm2 during calcium stimulation, P < 0.001]. Allografts had resting membrane potential depolarization and reduced action potential amplitude and upstroke velocity. iNOS mRNA was expressed in infiltrating inflammatory cells but not in allograft myocytes, endothelial cells, or isografts. Corticosteroids attenuated allograft contractile and electrophysiological dysfunction and inhibited iNOS enzyme activity. Direct iNOS inhibition with aminoguanidine inhibited NO production and prevented allograft contractile and electrophysiological dysfunction (e.g., tension of 64 mN/mm2 during calcium stimulation, P < 0.001). We conclude that 1) early allograft rejection caused contractile and electrophysiological dysfunction that was largely mediated by iNOS expression in infiltrating inflammatory cells, 2) corticosteroid-mediated amelioration of allograft contractile and electrophysiological dysfunction may reflect inhibition of iNOS, and 3) iNOS inhibition may offer an alternative in management of immune-mediated myocardial dysfunction.

Action Potentials↗
PubMedDate not supplied

[Autoimmune panhemopathy in lymphoid hyperplasia in a child].

The case reported concerns a 12 year old boy, admitted in 1970 with a clinical picture evoking a malignant hemopathy: thrombocytopenic purpura, leukopenia, multiple lymphadenopathies, enlarged spleen and, at histological examination, lympho-reticular hyperplasia of the spleen and lymphe nodes, simulating at the beginning, a nodular lymphoma. Immuno-hematological investigations revealed a complex auto-immune picture, which concerned essentially hematopoiesis. In fact, the pseudo-tumoral aspect of lymphenodes, was related to a dysfunction of the immune system, the pathogeny of which is presently better known.

Autoimmune Diseases↗
PubMed1994

[The chronic fatigue syndrome].

CFIDS (chronic fatigue and immune disfunction syndrome) is also known as CFS (chronic fatigue syndrome), CEBV (chronic Epstein-Barr virus), M.E. (myalgic encephalomyelitis), yuppie flu and by other names. It is a complex illness characterized by incapacitating fatigue (experienced as exhaustion and extremely poor stamina), neurological problems and a constellation of symptoms that can resemble many disorders, including; mononucleosis, multiple sclerosis, fibromyalgia, AIDS-related complex (ARC) and autoimmune diseases such as lupus. These symptoms tend to wax and wane, but any often severely debilitating and may last for many months or years. All sections of the population (including children) are at risk, but women under 45 seem to be most susceptible. The investigators suggest that CFIDS results from dysfunction of the immune system. The exact nature of this dysfunction is not yet well defined, but it can generally be viewed as an unregulated or overactive state which is responsible for most of the symptoms. There is also evidence of some immune suppression in CFIDS. None of the treatments is consistently satisfactory, but some may be helpful: psychotherapy, physiotherapy, exercise programs, acupunctures, small doses of antidepressants, etc.

Diagnosis, Differential↗
PubMed1988

Frequency of myocarditis, left ventricular dysfunction and ventricular tachycardia in the acquired immune deficiency syndrome.

To evaluate possible relations between clinical and histopathologic cardiac findings in patients with the acquired immune deficiency syndrome (AIDS), 58 consecutively autopsied AIDS patients were reviewed retrospectively. Twenty-six (45%) had histopathologic myocarditis. Fifteen of these 26 (58%) had greater than or equal to 1 clinical cardiac abnormalities: 6 had congestive heart failure or left ventricular (LV) dysfunction, or both, 4 had ventricular tachycardia (VT), 10 had electrocardiographic abnormalities and 4 had pericardial abnormalities. Of the 32 patients without myocarditis, 6 (19%) had pericardial or electrocardiographic abnormalities, or both, but none had congestive heart failure, LV dysfunction or VT. Overall, clinical cardiac abnormalities were found in 21 patients (36%). Patients with myocarditis had a significantly higher incidence of clinical cardiac abnormalities than patients without myocarditis (58 vs 19%, p less than 0.01). All patients with congestive heart failure, LV dysfunction or VT had myocarditis. Thus, serious clinical cardiac abnormalities were common in patients with AIDS and were associated with myocarditis.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Immune dysregulation in allergic respiratory disease: the role of T regulatory cells.

Although earlier research focused on the role of the polarity of T helper cell signalling as the defining factor in immune responses, it is now recognised that other cells with regulatory properties have a more key role. It has been recently proposed that allergic disease may result from an inappropriate balance between regulatory cells (including but not limited to CD4+ CD25+ T regulatory cells) and T helper type 2 (Th2) effector cells. In the airways, a number of other cells also have important regulatory effects on local immune responses, including epithelial cells and airway dendritic cells (DC). Allergic respiratory disease appears to be the culmination of both local epithelial dysfunction and generalised immune dysregulation resulting in Th2 propensity (atopic predisposition). Although these processes are related they also appear to occur independently. This review examines evolving models of allergy pathogenesis, including the newly recognised role of diverse groups of regulatory cells. Increasing rates of allergic disease (and other immune diseases) suggest that environmental changes may be having fundamental effects on common regulatory pathways. Understanding these influences and their mechanism of action could lead to strategies to prevent disease.

Animals↗
PubMed1990

HSV-1 enhances GvHR-associated parent anti-F1 alloreactivity in vivo and in vitro.

The present studies were performed to demonstrate whether concurrent HSV-1 infection could enhance the immune alterations and dysfunction associated with P----F1-induced graft-versus-host reactions. Examination of phenotypic and functional parameters revealed that Gv-HR-related immune abnormalities in the (C3H.SW X H-2bm1)F1 recipient were dependent on the parental donor inoculum. Together with HSV-1 infection, virus was found to exacerbate the phenotypic changes and functional abnormalities induced in this GvHR model. In addition, the presence of concurrent HSV-1 was shown to augment the level of specific in vivo donor anti-host reactivity present in F1 recipient spleen cells. Moreover, in vitro studies demonstrated that HSV-1 also enhanced the levels of parent anti-F1 allospecific cytotoxic activity. In total, these findings support the hypothesis that viral exacerbation of GvHR is mediated by its enhancement of donor anti-host alloreactive responses.

Animals↗
PubMed1999

Cryoglobulinemia.

Cryoglobulinemia may be found in a spectrum of disorders spanning clear-cut-B-cell neoplastic states, in which cryoprecipitation manifests as ischemic or occlusive vasculopathy, to a variety of immune complex diseases, in which vasculitis or glomerulonephritis may occur. Symptomatic cryoglobulinemia is many diseases, driven by and driving antibody-antigen responses, hepatic dysfunction, lymphoproliferation, and immune complexes. Distinguishing features that cause only some cryoglobulins to be symptomatic, elucidating the pathogenic mechanisms of HCV in cryoglobulin formation, and devising better therapies and more systematic evaluation of existing therapies are among the challenges for the future. Prognostication and classification will continue to rely on Brouet's classification (types I, II, and III), but additional features will probably include the presence or absence of HCV, HCV factors (genotype, titer), coexisting infections, B-cell clone burden, host factors, and immune system interactions (B- and T-cell idiotype networks, cytokines). Although antiviral therapy is a reasonable option for HCV-associated cryoglobulinemia, not all patients are HCV-positive, and only 60% to 80% of HCV-positive patients respond to IFN. In addition, not all patients tolerate IFN, and in those who do, the response is often short-lived once the treatment is discontinued. Only creative strategies, systematically studied, will provide long-awaited solutions.

Antigen-Antibody Complex↗
PubMedDate not supplied

[Metabolic role of glutamine and its importance in nutritional therapy].

The advances in the field of nutritional support have made certain nutrients very relevant, which, although they have been known for a long time, at present represent an important chapter in nutrition, entering into what is known as "nutritional pharmacology". Among these nutrients is glutamine, an amino acid classified as non-essential, but which in certain circumstances may become to be considered as an "essential nutrient". In the present review, a review is made of its metabolic role, synthesis and degradation, metabolic routes and functions under normal conditions as well as under critical conditions. It is known that glutamine stimulates the synthesis and inhibits the degradation of proteins, it is an important vehicle for the transport of nitrogen and carbon within the tissues, it stimulates the synthesis of hepatic glycogen, it is an energy source for cell division, for the growth of different cells of rapid replication, such as enterocytes, colonocytes, and fibroblasts, as well as for other cells of the immune system, such as lymphocytes and macrophages. Thus its role in the maintenance of structure, in metabolism and function of the intestinal mucosa, and in dysfunctions of the immune system. In parenteral nutrition, at present there are no preparations which include it, given the stability problems which it presents, although attempts have been made to resolve this, using different possibilities, such as di-peptides. However, in enteral nutrition, the diets tend to include it, although in a small proportion. Nevertheless, having recognized its beneficial role in a certain type of patients, at present there are diets which contain glutamine in higher doses, with the object of attempting to cover the increased demands of glutamine which shall arise in these situations. The inclusion of glutamine in nutritional therapy is supported by multiple studies which reflect the beneficial effect of this nutrient, both in enteral nutrition as in parenteral nutrition.

Bacterial Translocation↗
PubMed2001

Reconstitution of CD4+ T lymphocytes in HIV-infected individuals following antiretroviral therapy.

Immune reconstitution during antiretroviral therapy has recently been shown to depend upon multiple factors at work in T cell homeostasis, amongst which the reduction of thymus dysfunction and of immune hyperactivation are instrumental. The optimism that has been raised by the restoration of hosts' defenses against opportunistic pathogens is, however, balanced by the poor immunity restored against HIV; thus, innovative immune interventions are required.

Antiretroviral Therapy, Highly Active↗
PubMed2004

Graves' disease during immune reconstitution after highly active antiretroviral therapy for HIV infection: evidence of thymic dysfunction.

A patient with HIV infection who experienced immune reconstitution after highly active antiretroviral therapy (HAART) [increase in CD4 T cell count from <1/microl to >600/microl] presented with severe Graves' disease 32 months after commencing HAART. A comprehensive clinical and laboratory study demonstrated pronounced regional lymphadenopathy and thymic enlargement at presentation, and that the onset of thyrotropin receptor antibody production was associated with increased production of soluble CD30 (a marker of type 2 immune responses). Blood naive CD8 T cell counts and TREC levels in both CD4 and CD8 T cells were increased at multiple time points compared with carefully selected controls. We conclude that the Graves' disease in this patient was associated with abnormally high blood counts of thymus-derived T cells, and propose that Graves' disease after HAART in this and other HIV patients may result from failure to delete autoreactive T cell clones in the regenerating thymus.

Adult↗
PubMed2002

Plasticity of lymphoid compartments during HIV infection and treatments: hopes and limits.

Immune reconstitution during antiretroviral therapy has recently been shown to depend upon multiple factors at work in T-cell homeostasis, amongst which the reduction of thymus dysfunction and of immune hyperactivation is instrumental. The restoration of host defenses against opportunistic pathogens is, however, balanced by the poor immunity restored against HIV thus giving a satisfying link between antigen stimulation and the reconstitution of immune responses to pathogens.

Anti-HIV Agents↗
PubMed1988

Cellular immune reactions and blood cerebrospinal fluid barrier dysfunction in guinea pigs.

Both young and adult strain 13 guinea pigs have been treated with complete Freund's adjuvant (CFA). In young animals CFA induced an increase in the lymphocyte cell count in blood and a reversible blood CSF barrier impairment. Both these effects could be suppressed by the immunosuppressant drug Cyclosporin A. In contrast to the young animals treatment with CFA in adult strain 13 guinea pigs influenced neither the lymphocyte cell count nor blood CSF barrier function. In young and adult CFA-treated animals the number of polymorphonuclear cells in blood were increased and this increase was not reversed by Cyclosporin A. We discuss the influence of a systemic immune stimulation and suppression on blood CSF barrier function for proteins and its relevance to the pathogenesis of inflammatory diseases of the central nervous system.

Animals↗

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