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Results for “Immune dysfunction”

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PubMed1996

Consequences of hypogammaglobulinemia and steroid therapy in severe bronchopulmonary dysplasia.

We retrospectively studied the relation between corticasteroid therapy, hypogammaglobulinemia (HG), and recurrent infections in 37 infants with moderate to severe bronchopulmonary dysplasia (BPD). Nineteen of the 37 patients had tracheostomies because of chronic respiratory failure. We hypothesized that recurrent infections were most prevalent in infants whose IgG levels remained low at one year of age (persistent HG) and in infants receiving high doses of corticosteroids during the first year of life. We further hypothesized that the duration of HG was strongly correlated with the cumulative first year steroid dose. We also studied the response to intravenous gammaglobulin (IVIG) replacement therapy in this population of BPD infants. Our results showed an association between first year corticosteroid dose, duration of HG (r = 0.49, p < 0.003), and frequency of infections (r = 0.51, p < 0.001). We noted a relatively strong correlation between frequency of infections and duration of HG (r = 0.84, p < 0.0001). Twenty-four of 37 (65%) infants showed persistent HG and 49% had evidence of abnormal specific antibody production. Sixty-four percent of infants studied had reduced lymphocyte responsiveness to mitogen stimulation. Nineteen of 37 (51%) infants required IVIG for an average duration of 17.9 months due to recurrent infections. The average number of infections per year decreased from 10.6 to 2.8 (t = 12.32, p < 0.0001). There were no complications associated with IVIG therapy, but one infant died of bronchiolitis obliterans following heart-lung transplantation. Eight of 37 (22%) infants have persistent immunologic dysfunction requiring ongoing IVIG at four years or more of follow-up. We conclude that a substantial number of ill infants with BPD will have immune dysfunction characterized by persistently low IgG levels and reduced specific antibody responsiveness to protein antigens. We speculate that these findings are related to the cumulative dose of corticosteroids received in the first year of life and to the severity of underlying disease.

Adrenal Cortex Hormones↗
PubMed1993

Immune system of the spontaneously hypertensive rat: II. Morphology and function.

The spontaneously hypertensive rat (SHR) is a stress-sensitive animal which exhibits moderate immune dysfunction that has been implicated in the onset of hypertension. In this study, we examined the morphology of SHR thymus and spleen and further characterized the immune deficiency using Wistar-Kyoto (WKY) and Fisher 344 (F-344) rats for comparison. The adult SHR thymus does not display the increase in medullary volume typically noted with aging and the volume density of the marginal zone is decreased in the spleen. In vivo tritiated-thymidine incorporation is also decreased in the spleen of unstimulated SHR. In mixed lymphocyte reactions (MLR), the proliferative response of SHR splenocytes is significantly decreased relative to controls, WKY and F-344. Addition of interleukin-1 (IL-1), interleukin-2 (IL-2), or indomethacin to the MLR cultures does not increase proliferation. The proliferative response to T cell receptor monoclonal antibody (mAb-TCR) or interleukin-2 (IL-2) are similarly impaired in the SHR. The depressed proliferative T cell response is reversed by prolactin. It is suggested that the SHR is a valuable model for the study of immune deficiency.

Animals↗
PubMed1995

Behaviour of zinc in physical exercise: a special reference to immunity and fatigue.

The variations in plasma zinc levels is dependent which follows intensivity of exercise. It is clear that there are short-term effects of exercise on zinc metabolism. It has also been shown that a high level of constant exercise can have long-term effects on zinc metabolism. It has been reported that runners have lower plasma zinc levels than controls. Long term endurance training has been shown to significantly decrease resting serum zinc levels in both male and female athletes compared to sedentary controls. Severe zinc deficiency can affect muscle function. One consequence of low serum zinc levels could be a reduction in muscle zinc concentrations. Since zinc is required for the activity of several enzymes in energy metabolism it could be predicted that low muscle zinc levels would result in a reduction in endurance capacity. Zinc may also be acting directly at membrane level; changes in extracellular zinc levels have been reported to influence twitch-tension relationship in muscle. Some investigators have associated acute and exhaustive exercise with decreased immune function. The mechanisms by which physical stress modulates immune competence are complex, involving both immune and neuroendocrine messengers. Muscular fatigue is of critical importance and as such it has been the subject matter of numerous investigators. Although many factors have been identified, a clear cause remains elusive. Factors discussed include: energy supply, the accumulation of metabolites, eccentric work, immune dysfunctions, etc. Recently we have demonstrated that daily high and maintained physical training over a prolonged period of time (7 mo) provokes marked modifications in the immune system of elite sportsmen accompanied by a psychological and biochemical stress level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

The SLAM family of immune-cell receptors.

The 'signalling lymphocyte activation molecule' (SLAM) family is a newly appreciated group of immune-cell specific receptors that has the ability to regulate the function of several immune cell types. Recent studies show that the SLAM-related receptors mediate intracellular protein tyrosine phosphorylation signals. This property is dependent on the aptitude of SLAM-family receptors to bind with high affinity to SAP and/or EAT-2, two small adaptor molecules composed almost exclusively of a Src homology 2 domain. SAP is mutated in X-linked lymphoproliferative disease, a human immune dysfunction characterised by an inappropriate response to Epstein-Barr virus infection, thereby suggesting that the SLAM-related receptors may be critical for a normal immune response. The existence of the SLAM family broadens the spectrum of receptors known to be involved in immunomodulation.

Adaptor Proteins, Signal Transducing↗
PubMed1998

Primary Mycobacterium avium complex infections correlate with lowered cellular immune reactivity in Matschie's tree kangaroos (Dendrolagus matschiei).

The National Zoological Park has maintained a breeding colony of Matschie's tree kangaroos (Dendrolagus matschiei) since 1975 with a documented history and continued prevalence of Mycobacterium avium complex (MAC) infections. No evidence of immunosuppressive retrovirus infections or loss of heterozygosity that may have led to an immune dysfunction in these animals was found. Isolates of MAC organisms from affected tree kangaroos and from their environment had no common restriction fragment DNA types. Cellular immune reactivity in apparently healthy tree kangaroos was 3- to 6-fold lower than in humans and other marsupial and eutherian mammals, as determined by lymphocyte proliferative assays. Thus, while MAC infections are typically opportunistic in humans and other mammals, tree kangaroos commonly develop primary progressive disease with MAC from random sources. Comparative information derived from this study should benefit both the endangered tree kangaroo and humans with immunosuppressive disorders that lead to mycobacterial infections.

Animals↗
PubMed1993

High spontaneous intrachromosomal recombination rates in ataxia-telangiectasia.

Ataxia-telangiectasia (A-T) is an inherited human disease associated with neurologic degeneration, immune dysfunction, and high cancer risk. It has been proposed that the underlying abnormality in A-T is a defect in genetic recombination that interferes with immune gene rearrangements and the repair of DNA damage. Recombination was studied in A-T and control human fibroblast lines by means of two recombination vectors. Unexpectedly, spontaneous intrachromosomal recombination rates were 30 to 200 times higher in A-T fibroblast lines than in normal cells, whereas extrachromosomal recombination frequencies were near normal. Increased recombination is thus a component of genetic instability in A-T and may contribute to the cancer risk seen in A-T patients.

Animals↗
PubMed1985

Therapeutic considerations for use of immunomodulators in the treatment of ataxia-telangiectasia.

The nature of the soluble mediators of immune regulation, the lymphokines, is now being determined and this allows consideration of new approaches to treatment of disorders involving immune dysfunction, such as ataxia-telangiectasia. The immunomodulatory effects of interleukin-2, interferons, and known chemotherapeutic agents such as cyclophosphamide are considered in relation to the immune disorders of ataxia-telangiectasia. The possible etiology of the disease and its treatment are considered in relation to the immunopathologic effects that are observed.

Ataxia Telangiectasia↗
PubMed1988

Unusual breast masses. The sequential development of mammary tuberculosis and Hodgkin's disease in a young woman.

A left breast mass developed in association with pulmonary tuberculosis in a woman 26 years of age. Eight years later, rapidly fatal Hodgkin's Disease with chest wall erosion by involved mediastinal nodes simulating a breast lump developed. Subsequently, a discrete breast mass due to mammary Hodgkin's disease developed. Involvement of the breast by both tuberculosis and Hodgkin's disease, two diseases often associated with immune dysfunction, in a patient with dysmorphic features and a strong family history of tuberculosis, raises the possibility of an underlying genetic defect. This defect probably involves the immune system.

Adult↗
PubMed2003

N-3 polyunsaturated fatty acids and inflammation: from molecular biology to the clinic.

The immune system is involved in host defense against infectious agents, tumor cells, and environmental insults. Inflammation is an important component of the early immunologic response. Inappropriate or dysfunctional immune responses underlie acute and chronic inflammatory diseases. The n-6 PUFA arachidonic acid (AA) is the precursor of prostaglandins, leukotrienes, and related compounds that have important roles in inflammation and in the regulation of immunity. Feeding fish oil results in partial replacement of AA in cell membranes by EPA. This leads to decreased production of AA-derived mediators, through several mechanisms, including decreased availability of AA, competition for cyclooxygenase (COX) and lipoxygenase (LOX) enzymes, and decreased expression of COX-2 and 5-LOX. This alone is a potentially beneficial anti-inflammatory effect of n-3 FA. However, n-3 FA have a number of other effects that might occur downstream of altered eicosanoid production or might be independent of this effect. For example, dietary fish oil results in suppressed production of proinflammatory cytokines and can modulate adhesion molecule expression. These effects occur at the level of altered gene expression. Fish oil feeding has been shown to ameliorate the symptoms of some animal models of autoimmune disease and to protect against the effects of endotoxin. Clinical studies have reported that oral fish oil supplementation has beneficial effects in rheumatoid arthritis and among some asthmatics, supporting the idea that the n-3 FA in fish oil are anti-inflammatory. There are indications that the inclusion of fish oil in enteral and parenteral formulae is beneficial to patients.

Animals↗
PubMed1995

Chronic intestinal candidiasis as a possible etiological factor in the chronic fatigue syndrome.

The chronic candidiasis syndrome, also known as the Candida-related complex, putatively caused by the overgrowth of Candida albicans in the gastrointestinal tract and secondarily in the genital organs, is briefly described. Patients with this disorder have many of the same symptoms as those with the chronic fatigue syndrome, except for the recurrent flu-like symptoms of the latter disorder. The positive response of a large number of patients with the chronic fatigue syndrome (CFS) to an oral antifungal agent and a diet for intestinal candidiasis has been described by another clinician. There is evidence that Candida albicans infection of the mucous membranes depresses T cell and natural killer (NK) cell function. Similar abnormalities of immune function are found in the CFS. The function of cytotoxic T cells, T helper cells, and NK cells is important in preventing reactivation of infections from Epstein-Barr virus, cytomegalovirus, and other herpesviruses. Reactivation of one or more of these viruses could lead to the expression of the flu-like symptoms in the CFS. Yet the immune dysfunction found in this disorder has been considered the primary underlying causal factor. It is proposed that chronic intestinal candidiasis may be an agent which leads to immune depression in many CFS patients and therefore that it could be a causal factor in CFS.

Antifungal Agents↗
PubMed2004

The immune response to bovine viral diarrhea virus: a constantly changing picture.

Bovine viral diarrhea virus (BVDV) is one of the major immuno-suppressive viruses of cattle. The effect on the innate and acquired immune system is unique and results in dramatic immune dysfunction. BVDV infection also has the ability to cause persistent infection (PI) in the developing fetus. This Pl syndrome creates a requirement for high levels of BVDV immunity from vaccines to prevent these infections. BVDV vaccines and their future development continue to be an enigma in the control of BVDV.

Animals↗
PubMed2005

Genetic variability in the immune-inflammatory response after major burn injury.

Thermal injury induces immune dysfunction and alters numerous physiological parameters. Studies have proposed that genetics influence the outcome after traumatic injury and/or sepsis, however, the contribution of genetics to the immune-inflammatory response postburn has not been investigated. In this study, mice of three distinct genetic backgrounds (C57BL/6NCrlBR, BALB/cAnNCrlBR, and 129S6/SvEvTac) were subjected to thermal injury or a sham procedure, and 3 days later, blood and splenic immune cells (splenocytes and macrophages) were isolated for analysis. Splenocytes from the C57BL/6NCrlBR strain displayed suppressed splenic T cell proliferation postinjury, whereas the other strains were unaffected. Burn injury also induced a shift toward a Th2-type T-cell response (suppressed IFN-gamma production) in the C57BL/6NCrlBR strain, but not in the other strains. Macrophages from C57BL/6NCrlBR and 129S6/SvEvTac mice were highly proinflammatory with elevated productive capacity for TNF-alpha and nitric oxide, whereas no such changes were observed in macrophages for BALB/cNCrlBR mice. C57BL/6NCRLBR macrophages produced increased IL-10 levels postburn, and BALB/cNCrlBR macrophages had suppressed IL-10 production postinjury. No differences in fasting blood glucose and insulin were observed after thermal injury. However, significant postburn weight loss was observed in the BALB/cNCrlBR and 129S6/SvEvTac strains, but not in the C57BL/6NCrlBR strain. In summary, these findings support the concept that the immune-inflammatory response postburn is influenced by genetic make-up. Further elucidation of the influence of genetics under such conditions is likely to contribute to the improvement in existing, and development of new, therapeutic regimes for burn patients.

Animals↗
PubMed2006

Trauma: the role of the innate immune system.

Immune dysfunction can provoke (multiple) organ failure in severely injured patients. This dysfunction manifests in two forms, which follow a biphasic pattern. During the first phase, in addition to the injury by trauma, organ damage is caused by the immune system during a systemic inflammatory response. During the second phase the patient is more susceptible for sepsis due to host defence failure (immune paralysis). The pathophysiological model outlined in this review encompasses etiological factors and the contribution of the innate immune system in the end organ damage. The etiological factors can be divided into intrinsic (genetic predisposition and physiological status) and extrinsic components (type of injury or "traumaload" and surgery or "intervention load"). Of all the factors, the intervention load is the only one which, can be altered by the attending emergency physician. Adjustment of the therapeutic approach and choice of the most appropriate treatment strategy can minimize the damage caused by the immune response and prevent the development of immunological paralysis. This review provides a pathophysiological basis for the damage control concept, in which a staged approach of surgery and post-traumatic immunomonitoring have become important aspects of the treatment protocol. The innate immune system is the main objective of immunomonitoring as it has the most prominent role in organ failure after trauma. Polymorphonuclear phagocytes and monocytes are the main effector-cells of the innate immune system in the processes that lead to organ failure. These cells are controlled by cytokines, chemokines, complement factors and specific tissue signals. The contribution of tissue barrier integrity and its interaction with the innate immune system is further evaluated.

Journal Article↗
PubMedDate not supplied

The itching, burning eye: diagnostic algorithm and management options.

The healthy ocular surface is a complex, composite unit that is essential for patient comfort and visual function. A number of components need to work in an integrated manner to ensure that this is achieved, and a variety of causes can result in the final common symptom complex that can be termed the itching, burning eye. Many of these causes may be due to relatively common and simple issues related to lid disease, allergies, tear dysfunction, excessive computer use, exposure to polluted environment, and convergence problems. However, a smaller group may have potentially more serious pathology due to causes such as underlying immune dysfunction, or tumors; rarely, intraocular conditions and some neurological causes may present with ocular redness and grittiness. Failure or delay in the diagnosis of these latter entities can result in significant morbidity to the eye. This article will clarify issues related to the functioning of the ocular surface, provide a diagnostic algorithm for managing these patients, and discuss the current knowledge in the management of these conditions once they are diagnosed. It is targeted at the practicing ophthalmologist and should help him or her to manage this problem effectively.

Algorithms↗
PubMed1998

Impairments in immune cell function in B cell chronic lymphocytic leukemia.

B cell chronic lymphocytic leukemia (B-CLL) is a common clonal B cell leukemia that is often accompanied by a multitude of immune abnormalities. Each immune defect may be linked to several of the common complications affecting B-CLL patients. Furthermore, the combined abnormalities constitute a significant immunodeficiency for each patient. Importantly, some of the immune dysfunctions are potentially very relevant to the in vivo survival status of the leukemic B cell. The elucidation of these abnormalities in the circulating non-malignant immune cells of B-CLL patients has generated important insights into the biology of the disease. This discussion reviews the immune abnormalities of the clonal malignant B cells, the polyclonal B cells, and the immunoregulatory T cells and natural killer cells in B-CLL. In addition, we indicate the potential for immunotherapeutic protocols as innovations in treating this disease.

Antibody Formation↗
PubMed2006

Treg control of antimicrobial T cell responses.

Immunity to microbes depends on the function of numerous cell types and their products. These include T cells with regulatory function (Treg) against the components of the immune system. Recently, there has been much discussion regarding the circumstances in which protective or tissue-damaging T cell responses to microbes are affected by the activity of Treg. These relationships range from situations in which the Treg response seems to contribute to immune dysfunction to those that minimize tissue damage caused by immunoinflammatory T cell reactions. In several parasitic infections, Treg maintain equilibrium to ensure parasite persistence, minimal tissue damage and immunity to re-infection. Recently, several unresolved questions about the role of Treg in microbial infections have been raised and discussed. Learning how to successfully manipulate Treg responses could result in more effective vaccines and immunomodulators.

Animals↗
PubMed2005

Patients with acute on chronic liver failure display "sepsis-like" immune paralysis.

BACKGROUND/AIMS: Cellular immune depression is linked to high mortality in sepsis, but has yet to be systematically analysed in liver cirrhosis. The aim of the present study was to directly compare functional immune parameters in patients with acute on chronic liver failure (ACLF), severe sepsis, and non-decompensated cirrhosis. METHODS: Patients with ACLF (n=27) were investigated at admission to a medical ICU. Patients with stable liver cirrhosis (n=24) and severe sepsis (n=31) served as control groups. In all subjects, serum levels of IL-6 and IL-10, ex vivo production of TNF-alpha in a whole blood assay, and monocyte surface HLA-DR expression were determined. RESULTS: In patients with ACLF or sepsis, ex vivo TNF-alpha production and HLA-DR expression were severely decreased compared to subjects with stable cirrhosis (both P<0.001). Contrary, IL-6 levels were highest in septic patients, followed by subjects with ACLF and cirrhotic patients (both P<0.05). Immune dysfunction in ACLF was independent of aetiology of liver cirrhosis and associated with high mortality. CONCLUSIONS: Patients with ACLF and severe sepsis show a similar degree of cellular immune depression. The reduced cellular immune function in subjects with ACLF might contribute to the increased infectious morbidity of these patients and provide a rational basis for prevention strategies.

Adult↗
PubMed2000

Prospective crossover trial of the influence of vitamin E-coated dialyzer membranes on T-cell activation and cytokine induction.

Cytokine induction by dialyzer membranes has been related to several acute and chronic side effects of hemodialysis treatment, among them being immune dysfunction and progressive atherosclerosis. Surface modification of cuprophane dialyzers with the antioxidant vitamin E is a new approach to enhance biocompatibility and improve cytokine levels, as well as immune function. Twenty-one patients undergoing treatment with hemophane (HE) dialyzers were enrolled onto a crossover study with a vitamin E-coated (VE) dialyzer or a synthetic polyamide (PA) dialyzer. In vitro assays of lymphocyte activation and measurements of cytokine induction were performed to evaluate biocompatibility. Four weeks of treatment with either VE or PA dialyzers enhanced in vitro proliferation of peripheral blood leukocytes in comparison to treatment with HE membranes used before study entry. Enhancement of lymphocyte function was independent of dialysis efficiency, which was kept constant during the study. In the interdialytic interval, preactivation of monocytes for the production of interleukin-6 (IL-6) did not differ between VE or PA dialysis. In contrast, the VE membrane reduced acute production of IL-6 during a dialysis treatment, whereas the PA membrane did not. Unlike IL-6, the regulatory cytokine IL-10 is not inhibited by either membrane. This is important because IL-10 is believed to have a beneficial effect on immune function in dialysis patients. The VE membrane, despite being based on a cuprophane backbone, is similar to the highly biocompatible PA dialyzer in terms of its effect on lymphocyte function, whereas it exerts an additional suppressive effect on the overproduction of proinflammatory cytokines.

Aged↗