Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immune dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,621 records · Page 90Linked to original sources

Modelling human diseases in Drosophila and Caenorhabditis.

Drosophila (fruitfly) and Caenorhabditis (nematode worm) are useful model organisms for understanding many molecular and cellular mechanisms of human disease. Work on them is powered by versatile gene discovery methods, output of their genome projects, and a biology that has much in common with that of humans. They contain homologues of most human disease genes. Many aspects of human disease, and of defences against disease, are also found in flies and worms. These include cancer, ageing, neurodegeneration, infectious disease, innate immunity, and dysfunction of neurotransmitter and endocrine systems.

Animals↗

Clinical and immunologic approach to patients with alleged environmental injury.

Many of the challenging clinical evaluations facing today's practitioner and particularly today's allergist involve suspected hidden environmental exposure, not only to traditional allergens that induce classic symptoms of IgE-mediated disease, but to a wide range of simple chemicals encountered in trace amounts that may be associated with multisystemic symptoms including behavioral and neurologic manifestations. In the litigious social climate in which we live, the increased number of disability and personal injury claims and the ambiguous posturing by the legal profession often dictate a new set of diagnostic rules and norms. These must be considered by allergists and other practitioners in evaluating patients with polysomatic complaints allegedly due to trace environmental contaminants and with little or no identifiable pathology by gross or microscopic examination of tissues or laboratory data. These patients may have been declared totally disabled and may be seeking or receiving large amounts of personal injury compensation. Furthermore, they may be under "treatment" with multiple unproven diagnostic and therapeutic modalities and properly controlled challenge procedures may be necessary to prove or disprove the necessity for these diagnostic tests and therapies. With the ever increasing industrialization of our environment, it is likely that patients with these problems, who present for evaluation, will increase in number. It is therefore prudent for the practitioner to consider sound, comprehensive approaches to diagnoses and management of these conditions and above all to allay morbid fears of clinically relevant disease or immune system dysfunction based on results of isolated laboratory test findings.

Drug Hypersensitivity↗

L-arginine improves wound healing after trauma-hemorrhage by increasing collagen synthesis.

BACKGROUND: Several studies indicate impaired wound healing after trauma and shock. Wound immune cell dysfunction seems to be responsible for altered wound healing after trauma-hemorrhage (T-H). In this respect, administration of the amino acid L-arginine normalized wound immune cell function under those conditions. It remains unknown, however, whether L-arginine improves impaired wound healing after T-H. METHODS: To study this, male C3H/HeN mice were subjected to a midline laparotomy (i.e., soft tissue trauma induced), and polyvinyl sponges were implanted subcutaneously at the wound site before hemorrhage (35 +/- 5 mm Hg for 90 minutes) or were subjected to sham operation. During resuscitation, mice received 300 mg/kg body weight L-arginine or saline (vehicle). Seven days thereafter, hydroxyproline (OHP), a metabolite of collagen synthesis, was measured in the wound fluid using high-performance liquid chromatography. Collagen types I and III were determined in the wound by Western blot analysis. In addition, wound breaking strength was measured 10 days after T-H or sham operation. RESULTS: The results indicate that OHP was significantly decreased in T-H mice. L-arginine, however, restored depressed OHP in the wound fluid in the T-H animals. Similarly, L-arginine treatment prevented a significant depression of collagen I synthesis after T-H. Collagen III was not significantly affected by T-H or L-arginine. Most important, L-arginine increased maximal wound breaking strength after severe blood loss. Therefore, L-arginine improves wound healing after T-H by increasing collagen synthesis. CONCLUSION: Because L-arginine improves wound healing, the results suggest that L-arginine might represent a novel and useful adjunct to fluid resuscitation for decreasing wound complications after trauma and severe blood loss.

Analysis of Variance↗

Nitric oxide reduces bacterial superantigen-immune cell activation and consequent epithelial abnormalities.

Inhibition of the inducible form of nitric oxide (NO) synthase prolonged the murine enteropathy evoked by the bacterial superantigen, Staphylococcus aureus enterotoxin B (SEB). We examined the ability of NO to alleviate SEB-induced epithelial dysfunction and immune cell activation. Human peripheral blood mononuclear cells (PBMC) were activated by SEB for 24 h +/- the NO donors, S-nitroso-N-acetylpenicillamine and spermine-NONOate. The conditioned medium (CM) was collected and applied to T84 epithelial monolayers, and permeability [i.e., transepithelial resistance (TER)] and stimulated ion transport (i.e., short-circuit current responses to carbachol and forskolin) were assessed 24 h later. Exposure to CM led to an approximately 40% drop in TER and hyporesponsiveness to both secretagogues. CM made in the presence of NO donors (10(-4) M) had no significant effect on epithelial barrier or ion transport parameters. NO donors alone had no effect on naive epithelia, and addition of the NO donors to previously made CM did not affect the ability of this CM to alter epithelial function. Moreover, the NO donors dose-dependently reduced SEB-evoked PBMC proliferation and cytokine production (i.e., interferon-gamma, tumor necrosis factor alpha) but did not affect viability. These findings suggest a beneficial role for NO in inflammation by reducing immune cell activation and thus ameliorating consequent physiological abnormalities, in this instance, perturbed epithelial permeability and active ion transport.

Antigens, Bacterial↗

The immune system in the oxidative stress conditions of aging and hypertension: favorable effects of antioxidants and physical exercise.

Several studies have shown that both oxidative stress and inflammation are linked to the process of hypertension and that the immune system is also involved in this age-related process. More specifically, the oxygen stress related to immune system dysfunction seems to have a key role in senescence, in agreement with the oxidation/ inflammation theory of aging. From a practical point of view, and according to our own research, the immune functions change in a similar fashion in hypertension and aging. As antioxidant diet supplementation decreases oxidative stress, it may be useful to treat hypertension and increase longevity. Probably, these favorable effects are mediated by an antioxidant-induced improvement of the immune function. The practice of moderate physical exercise shows similar favorable effects, and indeed our studies on exercising hypertensive women demonstrate an improved immune function, probably linked to raised levels of intracellular antioxidant defenses. The present review summarizes a selection of data related to the above from other authors as well as some findings from our own work.

Aging↗

Prophylactic measures in the solid-organ recipient before transplantation.

Pretransplant screening affords an important opportunity to detect and treat preexisting active infection in the solid-organ transplant recipient. In this article, pretransplant strategies for preventing infections after solid-organ transplantation are reviewed. In addition to the search for active preexisting infection in the transplant candidate, immunization remains a cornerstone of preventive practice. Because there is a suboptimal response to vaccinations in patients who are receiving immunosuppressive therapy, as well as in patients with end-stage organ dysfunction, standard immunization of the transplant candidate should be updated as early as possible in the course of the illness, including pneumococcal, influenza, and hepatitis B vaccines. Liver transplant candidates should receive hepatitis A vaccine, and children should receive Haemophilus influenzae type B conjugate vaccine. All nonimmune pretransplant patients should be considered candidates for the varicella vaccine. The management of special risk groups is discussed in detail.

Adult↗

Immunodeficiency associated with lymphosarcoma in a horse.

Immune system dysfunction and immunoglobulin deficiency was diagnosed in a 2-year-old horse with disseminated lymphosarcoma. Prolonged (35 days) parenteral nutrition was delivered to support the horse during a period in which immune function studies could be performed. Correction of nutritional compromise by use of parenteral nutrition did not correct the immunoglobulin deficiency, and results of lymphocyte phenotype testing did not indicate abnormal proportions of leukocytes. Lymphoblast transformation studies were suggestive of a circulating immunosuppressive factor in the horse's serum. Normal cell function was detected when the cells were stimulated in precolostral equine serum.

Animals↗

The presence of dominant T-cell clones in peripheral blood of patients with collagen vascular disorders: a prospective study of 97 cases.

BACKGROUND: T-lymphocyte dysfunction has been seldom investigated in collagen vascular disorders. The search for dominant T-cell clones has been scarcely reported, although the presence of such clones might be expected in disorders showing immune responses directed against a variety of autoantigens. OBJECTIVES: We conducted a systematic search for dominant T-cell clones in peripheral blood in patients with collagen vascular disorders. Patients and methods Ninety-seven patients with collagen vascular disorders were studied (7 cutaneous and 38 systemic lupus erythematosus; 8 multiple morphea; 12 regional scleroderma; 32 systemic sclerosis of the CREST type). A dominant T-cell clone was searched for in peripheral blood by polymerase chain reaction targeting the T-cell receptor gamma chain followed by a size analysis of amplified fragments. Peripheral blood from patients with nonlymphocyte-dependent disorders and matched by age and sex was assessed in the same conditions. Results in both groups were compared using nonparametric statistical tests. RESULTS: Overall, a circulating dominant T-cell clone was found in 52% of patients compared with 16.9% in controls. More precisely, such a dominant clone was present in 43% and 37% of cutaneous and systemic lupus erythematosus, respectively, in 75% of multiple morphea, 75% of regional scleroderma and 60% of CREST syndrome patients. The percentages in all subsets of patients were significantly higher than in the control group. CONCLUSIONS: The presence of a dominant T-cell clone in peripheral blood is significantly more frequent in collagen vascular disorders than in controls, especially in patients with scleroderma, whatever the clinical subset, which suggests T-cell involvement in the immune response dysfunction in these diseases classically characterized by disturbances of B lymphocytes. The relevance of such a dominant clone regarding diagnosis, pathomechanisms, long-term outcome and visceral prognosis of these diseases as well as therapeutic decisions remains to be evaluated.

Adolescent↗

The participation of antiviral immune mechanisms in alveolar macrophage dysfunction during viral pneumonia.

Virus infections transiently suppress pulmonary antibacterial defenses by causing dysfunctions in the alveolar macrophage phagocytic system. This impairment of pulmonary bactericidal activity is not associated in time with virus proliferation, but rather with the period of time of rapidly declining virus titers and the expression of the antiviral immune response in the lungs. This temporal relationship suggests that the impairment of pulmonary bactericidal activity might be secondary to the antiviral immune response rather than a direct effect of virus replication. Immune depletion of mice during the course of influenza virus pneumonia ameliorated the virus-induced bactericidal defect and prevented bacterial multiplication in the lungs. In contrast, immune reconstitution reestablished the alveolar macrophage phagocytic defect. These data indicate that virus-induced suppression of pulmonary antibacterial defenses may be, in part, immunologically mediated.

Animals↗

Plasticity of neuroendocrine-thymus interactions during ontogeny and ageing: role of zinc and arginine.

Thymic re-growth and reactivation of thymic functions may be achieved in old animals by different endocrinological or nutritional manipulations such as, (a) treatment with melatonin, (b) implantation of a growth hormone (GH) secreting tumour cell line (GH3 cells) or treatment with exogenous GH, (c) castration or treatment with exogenous luteinizing hormone-releasing hormone (LHRH), (d) treatment with exogenous thyroxin or triiodothyronine, and (e) nutritional interventions such as arginine or zinc supplementation. These data strongly suggest that thymic involution is a phenomenon secondary to age-related alterations in neuroendocrine-thymus interactions and that it is the disruption of these interactions in old age that is responsible for age-associated immune-neuroendocrine dysfunctions. The targets involved in hormones-induced thymic reconstitution may directly or indirectly involve hormone receptors, cytokines, arginine, and a trace element such as zinc, which is pivotal for the efficiency of neuroendocrine-immune network during the whole life of an organism. The effect of GH, thyroid hormones, and LHRH may be due to specific hormone receptors on thymocytes and on thymic epithelial cells (TECs), which synthesize thymic peptides. Melatonin may also act through specific receptors on T-cells. In this context, the role of zinc, which turnover is reduced in old age, is pivotal because of its involvement through zinc fingers in the gene expression of hormone receptors. In addition, the effects of zinc are multifaceted: from the reactivation of zinc-dependent enzymes, to cell proliferation and apoptosis, to cytokines expression and to the reactivation of thymulin, which is a zinc-dependent thymic hormone required for intrathymic T-cell differentiation and maturation as well as for the homing of stem cells into the thymus. Zinc is also required for arginine action, via NO pathway. The role of zinc is therefore crucial in neuroendocrine-thymus interactions. According to data in animals and humans, the above reported endocrinological manipulations (GH, thyroid hormones, and melatonin) or arginine treatment may also act via zinc pool in restoring thymic activity in ageing allowing improvements on peripheral immune efficiency.

Aging↗

The combined immunological and antinociceptive defects of beige-J mice: the possible existence of a 'mu-repressin'.

A selective non-responsiveness to the analgesic effects of opioid mu receptor-, but not opioid delta receptor-, mediated antinociception in the tail-flick test has been identified in C57BL/6J-bgJ (beige-J) mice. The beige-J mutation is also known to give rise to multiple immunological disorders and immune cell dysfunctions. A link between these apparently disparate manifestations has been examined in a series of studies using, for example, adoptive transfer of spleen cells. The findings appear to have broad implications for the link between the immune and opioid systems.

Animals↗

The use of immunoglobulins in the treatment of human epilepsy.

The use of immunoglobulin (IVIg) in intractable epilepsy is one of its oldest applications in medicine, starting from the empirical observation of its beneficial effect on seizures. Immune system dysfunction may play a role in epilepsy by triggering, maintaining or, unexpectedly, improving intractable seizures. Several laboratory and clinical investigations are in favor of an immunological basis for different forms of experimental and human epilepsies. A wide range of immune abnormalities have been reported, suggesting the existence of different subtypes of epileptic syndromes with different abnormalities of the immune system. In this view, IVIg with its broad immunomodulatory mechanism of action could be effective in different forms of immune-dysregulated intractable epilepsies. Non-immunological mechanisms of action have been also suggested, based either on human epilepsy data or on animal experimental data. The possible anticonvulsant properties and the ability of IVIg to interfere with the final common pathway of seizures at a cellular level, with a significant increase in seizure threshold, have been demonstrated in different experimental epilepsy model. Although IVIg may represent a valuable resource in some drug-refractory epilepsies and its effectiveness has important pathogenetic implications, controlled studies with the systematic monitoring of immunological markers are needed to define more precise indications and to optimize the administration protocols.

Blood-Brain Barrier↗

Two patients with heparin-induced thrombocytopenia followed by idiopathic (immune) thrombocytopenic purpura: case report.

Heparin-induced thrombocytopenia (HIT) and idiopathic thrombocytopenic purpura (ITP) are separate and well-recognized clinical syndromes, 10both having potential for disastrous outcomes. Sequential occurrence of these two diseases has not been reported in the literature. We report herein two patients who were initially diagnosed as having HIT but whose later clinical course was similar to ITP. Although dysfunction of immune system seems to play a role, the precise mechanisms for the development of these diseases are unclear. As both conditions have different natural histories and require different treatment modalities, it is important to recognize that these two diseases may be seen sequentially.

Adult↗

Intestinal malabsorption of HIV-infected children: relationship to diarrhoea, failure to thrive, enteric micro-organisms and immune impairment. The Italian Paediatric Intestinal/HIV Study Group.

OBJECTIVE: To determine the features and the prevalence of intestinal-dysfunction in HIV-infected children and to investigate its relationship to diarrhoea, growth failure, immune dysfunction and enteric pathogens. DESIGN: Case controlled, cross-sectional multicentre study. SETTING: Children enrolled in tertiary care Italian centres for paediatric HIV infection from June 1990 to June 1992. Intestinal function tests and investigation for enteric viruses were performed in Naples. PATIENTS: Forty-seven children with symptomatic HIV infection, six of whom had diarrhoea. Fifty non-infected children with diarrhoea and 48 healthy children were enrolled as controls for enteric viruses positivity and intestinal tests. METHODS: Intestinal function was investigated by measuring fat, protein and carbohydrate adsorption using the steatocrit method, and determining the faecal concentration alpha-1-antitrypsin and the d-xylose absorption, respectively. Microbiological studies included investigation for classical and opportunistic pathogens and for enteric viruses by electron microscopy in the stools of HIV-infected children. The presence of viruses in the stools of HIV-negative children was also investigated. RESULTS: A high prevalence of intestinal-dysfunction was detected in HIV-infected children; faecal fat loss was detected in 14 out of 47 (30%), carbohydrate malabsorption in 15 out of 47 (32%) and protein loss in eight out of 47 (17%) HIV-infected children. Mean values of xylose blood level and of steatocrit were significantly different from those of healthy controls. Four children with diarrhoea were positive for Cryptosporidium. The prevalence of enteric viruses was significantly increased in HIV-infected children (57%) compared with healthy controls (17%). Intestinal-dysfunction was not associated with diarrhoea, poor growth, enteric agents or degree of immune dysfunction. CONCLUSIONS: Intestinal-dysfunction, consisting of fat, carbohydrate and protein malabsorption, is a common feature of paediatric HIV infection. Although not clinically evident, it may contribute to further worsening of the disease.

Adolescent↗

Topical and systemic therapy for recurrent aphthous stomatitis.

The cause of recurrent aphthous ulcers (RAU), the lesions of recurrent aphthous stomatitis, is incompletely understood but appears to involve immune system dysfunction. Treatment options include no treatment, treatment of associated systemic diseases or conditions (eg, celiac sprue, vitamin deficiencies), systemic medications, topical medications, conversion of the aphthous ulcer to a wound, and palliative treatments. The most effective treatments (systemic or topical corticosteroids, thalidomide) involve agents that suppress or modulate immune system function. In general, topical agents are preferred because they have fewer associated side effects; however, inability to obtain adequate contact time may limit their effectiveness. Adjunct pain control is sometimes necessary, either with pain medications or with adherent agents that coat the ulcers.

Adjuvants, Immunologic↗

4. Autoimmunity, vasculitis, and autoantibodies.

Autoimmune diseases are distinct clinical syndromes characterized by various alterations in normal immune responsiveness, such that there is a loss of tolerance to particular host constituents. In most cases, despite years of intense investigation, the etiopathogenic antigens initiating these systemic inflammatory conditions remain undefined. However, a great deal has been learned about the changes in components of the immune response relevant to the propagation and sustenance of these often chronic disorders. In addition, various hormonal, environmental, physiologic, and other influences that affect their expression have been identified. The expression and ultimate clinical outcome of autoimmune diseases usually relate to inflammation-related damage to the target organ with subsequent dysfunction. Certain immune conditions, such as autoimmune thyroid disease, largely affect a single organ, whereas others, such as systemic lupus erythematosus, heterogeneously affect sundry organ systems. Autoantibodies directed against normal host antigens are a common feature of many autoimmune diseases. In some cases they are pathogenic, whereas in others they serve as markers for organ involvement or outcomes. Clinical descriptions of autoimmune diseases date back many decades in some cases. Recent efforts at formulating classification criteria have allowed clearer distinctions and more accurate stratification. Greater understanding of the immunopathogenesis of autoimmune conditions has led to the development and introduction into the clinic of novel immunomodulatory therapies and treatment paradigms that have substantially improved the outcomes for patients affected by these serious conditions.

Animals↗

Neurocognitive and psychological contributions to quality of life in HIV-1-infected women.

OBJECTIVES: The purpose of this study was to examine the impact of neurocognitive and emotional distress and immune system dysfunction on quality of life in women with HIV. METHODS: Thirty-six HIV-seropositive women were administered measures of mood status (Profile of Mood States), quality of life (Multidimensional Quality of Life Questionnaire for Persons with HIV) and cognitive function. CD4 cell counts were obtained as an indicator of immune system status. RESULTS: Regression analyses revealed that independent of severity of emotional distress, neurocognitive deficits on measures of executive control and speed of information processing were associated with reduced quality of life. Emotional status also was associated with quality of life and together with neurocognitive performance accounted for most of the variance associated with quality of life. Reduced CD4 cell count was significantly associated with neurocognitive deficits, but not severity of emotional distress or quality of life. CONCLUSIONS: Quality of life among women who are infected with HIV is strongly influenced by both neurocognitive and emotional status, as women with the greatest neurocognitive impairment and emotional distress report the poorest quality of life.

Adult↗