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PubMed2003

Lower endotoxin immunity predicts increased cognitive dysfunction in elderly patients after cardiac surgery.

BACKGROUND AND PURPOSE: Although coronary artery bypass graft surgery (CABG) improves the quality of life and functional capacity for numerous patients, many also exhibit impairment in cognitive function immediately after surgery. Although the etiology of this cognitive decline is multifactorial, the inflammatory response to the primary insult may modulate the extent of dysfunction. Patients with low preoperative levels of anti-endotoxin core antibody (EndoCAb) are more likely to experience adverse outcomes, suggesting that decreased immunity to endotoxin causes a heightened release of inflammatory mediators. We therefore sought to determine the association of decreased EndoCAb and the incidence of postoperative cognitive decline. METHODS: EndoCAb levels were measured before surgery in 460 patients undergoing elective CABG. Cognitive function was measured preoperatively and 6 weeks postoperatively. Multivariable analysis accounted for the effects of age, Parsonnet score, sex, body mass index, baseline cognition, years of education, history of hypertension, bypass time, cross-clamp time, and number of grafts. RESULTS: At 6-week follow-up, 122 patients (36%) showed cognitive decline. Lower preoperative EndoCAb levels were associated with a greater incidence and severity of postoperative cognitive decline. The elderly with decreased endotoxin immunity are particularly susceptible to this decline (relative risk=1.97 for age >64). CONCLUSIONS: Reduced preoperative endotoxin immunity is a predictor of increased postoperative cognitive dysfunction in patients undergoing CABG, particularly in those >60 years old. Interventions that increase IgM EndoCAb levels might improve cognitive function after cardiac surgery.

Adult↗
PubMed1995

Surfactant dysfunction develops when the immunized guinea-pig is challenged with ovalbumin aerosol.

BACKGROUND: The cause of the airway resistance developing during an asthma attack is not completely understood. Besides bronchospasm and airway oedema a surfactant dysfunction has been suggested as a reason for an increased airway resistance. OBJECTIVE: This paper aims at examining if indeed surfactant dysfunction develops when an asthma attack is induced in guinea-pigs. METHODS: Guinea-pigs, immunized against ovalbumin and then challenged (by inhaling the antigen) underwent lung function tests (n = 7) and were compared with seven animals challenged, but not immunized. Lung lavage was carried out in three groups of guinea-pigs: controls, never immunized nor challenged (n = 7), not immunized but challenged (n = 6), immunized and challenged, no lung function test (n = 6). After concentrating the lavage fluid 10 times the surface activity was evaluated with the pulsating bubble surfactometer. The fluid's concentration of phospholipids and proteins was determined as was the phospholipid composition. RESULTS: The 19 immunized and challenged animals all developed severe respiratory distress, six so seriously that they died. Lung function tests showed significantly increased airway resistance and decreased tidal volume, minute volume, and dynamic compliance. Surface activity of lavage fluid from immunized and challenged animals was significantly reduced when compared with fluid from control animals (P < 0.01). Immunization and challenge had no effect on the lavage fluid's phospholipid concentration or composition, but the proteins were at a higher concentration than in the fluid of the controls (P < 0.01). CONCLUSION: Proteins leaking into the airways inhibited the surfactant. This, in turn might have caused conducting airways to become blocked by liquid columns, which would increase airway resistance.

Administration, Inhalation↗
PubMed2002

High prevalence of autoimmune thyroid disease in pulmonary arterial hypertension.

STUDY OBJECTIVES: An association between thyroid disease and pulmonary arterial hypertension (PAH) has been reported, yet the pathogenetic relationship between these conditions remains unclear. Because immune system dysfunction may underlie this association, we sought to determine the prevalence of autoimmune thyroid disease (AITD) in patients with PAH. DESIGN AND SETTING: Prospective observational study at a single academic institution. PATIENTS: Sixty-three consecutive adults with PAH (ie, sustained pulmonary artery systolic pressure, > 25 mm Hg) were evaluated for clinical, biochemical, and serologic features of AITD. MEASUREMENTS: Thyroid gland dysfunction was determined by clinical examination for goiter, and by biochemical measurements of thyrotropin and free thyroxine. Immune system dysfunction was determined by serologic measurements of antibodies to thyroglobulin and thyroid peroxidase. First-degree family history of AITD also was ascertained in order to investigate for genetic clustering of autoimmunity. RESULTS: Thirty-one patients (49%; 95% confidence interval [CI], 37 to 62%) received diagnoses of AITD. Eighteen patients were newly diagnosed, and 9 patients required the initiation of pharmacologic treatment. There was no chronologic relationship between the diagnosis or treatment of PAH and that of AITD. Sixteen patients (25%; 95% CI, 15 to 36%) had 24 first-degree family members with AITD. CONCLUSIONS: Approximately half of the patients with PAH have concomitant AITD. These two conditions may be linked by a common immunogenetic susceptibility, and the elucidation of this association may advance the understanding of the pathophysiology and treatment of PAH. Systematic surveillance for occult thyroid dysfunction in patients with PAH may prevent the hemodynamic exacerbation of right heart failure.

Adult↗
PubMedDate not supplied

Diet restriction impairs extracellular signal-regulated kinase activation of peritoneal exudative cells after N-formyl-methionyl-leucyl-phenylalanine stimulation in a murine peritonitis model.

BACKGROUND: Phosphorylation of extracellular signal-regulated kinase (ERK) enhances various inflammatory responses in immune cells. It is unknown whether dysfunction of immune cells during malnutrition is attributed to derangement of ERK activation. METHODS: Male Institute of Cancer Research (ICR) mice received chow (146 g/kg per day, ad libitum or 36.5 g/kg per day, diet-restricted) for 7 days. Mice (n = 55) were given 6.5 mg/kg of an ERK inhibitor (PD98059) or vehicle intraperitoneally (IP), at 2 hours before cecal ligation and puncture (CLP). Survival was observed up to 60 hours. Detection of phosphorylated ERK (pERK) in the peritoneal exudative cells (PECs) was done as follows. In a separate study, PECs were harvested by peritoneal lavage 2 hours after an IP injection of 1% glycogen. PECs were incubated with or without 100 nmol/L N-formyl-methionyl-leucyl-phenylalanine (fMLP) for 1 minute. PEC ERK activation was detected with Western blot analysis (n = 38), by densitometric quantification, and with a laser scanning cytometer (LSC; n = 13). Subpopulations of PECs were determined by Wright-Giemsa staining. Unstimulated pERK expression was normalized to 100% for Western blot analysis. RESULTS: Diet restriction reduced survival after CLP compared with the ad libitum mice. ERK inhibition showed no effect on survival in diet-restricted mice but reduced survival in ad libitum mice. There were no differences in subpopulations of PECs 2 hours after glycogen injection between the groups. Western blot analysis revealed that fMLP stimulation significantly increased the phosphorylation of ERK1/2 in PECs from the ad libitum group (ERK1, 199 +/- 41%; ERK2, 211 +/- 49%; p < .03) but not in those from diet-restricted mice (ERK1, 98 +/- 10%; ERK2, 91 +/- 9%). Mean fluorescence intensity (MFI) of pERK in PECs obtained by LSC was significantly elevated after fMLP in the ad libitum group (from 19.4 +/- 1.5 MFI to 22.4 +/- 1.2 MFI; p < .05) but did not change in the diet-restricted group (from 19.4 +/- 1.8 MFI to 19.1 +/- 1.5 MFI). CONCLUSIONS: ERK activation is essential for survival in this murine sepsis model. Impaired ERK activation of PECs may, at least in part, impair host defense during malnutrition.

Animals↗
PubMed2000

Microglia dysfunction in schizophrenia: an integrative theory.

Schizophrenia is a devastating illness of unknown etiology. It is characterized by increased brain ventricular volume, suggesting a progressive neurodevelopmental condition. There is evidence suggesting a correlation between in utero viral exposure and subsequent occurrence of schizophrenia. Many neurotransmitter systems have been implicated as being dysfunctional in schizophrenia. There are also data suggesting immune system dysfunction in schizophrenia, and a negative correlation between schizophrenia and rheumatoid arthritis. Microglia are phagocytic immune cells in the central nervous system (CNS) derived from peripheral blood monocytes. They are involved in brain development, neuroproliferative and neurodegenerative activities, several CNS illnesses, and CNS viral immunity. They may also be involved in neurotransmitter regulation. The current theory postulates microglial dysfunction initiated by early CNS viral exposure results in the abnormal neural development and neurotransmitter dysfunction seen in schizophrenia.

Brain↗
PubMed2004

Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome.

CONTEXT: Irritable bowel syndrome (IBS), which affects 11% to 14% of the population, is a puzzling condition with multiple models of pathophysiology including altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation. Although no conceptual framework accounts for all the symptoms and observations in IBS, a unifying explanation may exist since 92% of these patients share the symptom of bloating regardless of their predominant complaint. EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for relevant English-language articles beginning with those related to bloating, gas, and IBS. Bibliographies of pertinent articles and books were also scanned for additional suitable citations. EVIDENCE SYNTHESIS: The possibility that small intestinal bacterial overgrowth (SIBO) may explain bloating in IBS is supported by greater total hydrogen excretion after lactulose ingestion, a correlation between the pattern of bowel movement and the type of excreted gas, a prevalence of abnormal lactulose breath test in 84% of IBS patients, and a 75% improvement of IBS symptoms after eradication of SIBO. Altered gastrointestinal motility and sensation, changed activity of the central nervous system, and increased sympathetic drive and immune activation may be understood as consequences of the host response to SIBO. CONCLUSIONS: The gastrointestinal and immune effects of SIBO provide a possible unifying framework for understanding frequent observations in IBS, including postprandial bloating and distension, altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation.

Anti-Bacterial Agents↗
PubMed1992

Mononuclear leukocyte ADP-ribosylation as an indicator of immune function in malignant-glioma patients treated with betamethasone for cerebral edema.

Glioma patients receiving corticosteroids (16 mg/day betamethasone) were examined for evidence of immune cell dysfunction by using quantitative estimates of adenosine diphosphate (ADP)-ribosylation in peripheral mononuclear leukocytes as the physiological indicator. The duration of daily treatment with corticosteroids varied from 0 to 35 days at the time of collection of the blood samples. Even after adjustment for covariate factors such as age, sex, smoking habits, alcohol use, antiepileptic medications, and tumor grade, there still remained a highly significant dose-dependent inverse relationship between constitutive and hydrogen peroxide-induced mononuclear leukocyte ADP-ribosylation levels and the duration of corticosteroid treatment (beta coefficients -0.40 and -0.29, respectively; p less than 0.03). No other variable under consideration significantly influenced ADP-ribosylation levels after statistical adjustment. These data support a mutual interdependence of mononuclear leukocyte ADP-ribosylation and corticosteroid-induced immune cell dysfunction in vivo.

Betamethasone↗
PubMed2001

Humoral immune response to cruzipain and cardiac dysfunction in chronic Chagas disease.

The humoral immune response to epitopes expressed on cruzipain was evaluated in 31 Chagas disease patients (CDP) with different degrees of cardiac dysfunction. We took advantage of the availability of anti-Trypanosoma cruzi microsomal fraction monoclonal antibodies (MoAbs) reactive with epitopes that are recognized (5A9B11) or not recognized (1A10C11) by CDP sera. The 5A9B11- and 1A10C11-like epitopes are expressed on cruzipain. The reactivity of 5A9B11 against cruzipain was completely inhibited by sera of severe cardiopathy patients while a partial inhibition was found with sera from chagasic patients with mild disease. CDP sera did not block cruzipain recognition by 1A10C11. The antigenic determinants recognized by CDP sera appeared to be linear and carbohydrate free. When the overall anti-cruzipain immune response was evaluated, 70% of CDP with severe disease showed cruzipain titers higher than 1/800 while none of them displayed titers lower that 1/400. This report shows for the first time that the humoral immune response against epitopes expressed on cruzipain appeared to be related with the severity of chronic Chagas disease.

Adult↗
PubMed2004

Immune system-mediated endothelial damage is associated with NO and antioxidant system disorders.

Two distinct systems of different origin are involved in the pathogenesis of both infectious and immunological vasculitis syndrome: nitric oxide (NO) from endothelial cells and granulocyte NADPH oxidase. In this study, in 31 children with immune system dysfunction, NO, NO synthase (NOS) and antioxidant enzyme activities [catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx)], as well as immunological parameters, were investigated. On the basis of the clinical findings, all children were divided into three groups: group I, 8 children clinically showing macular skin manifestations; group II, 11 children with maculo-papulous changes; and group III, 12 children with clinical findings of papulous changes. Plasma NO values in groups II and III were significantly elevated (79.14+/-30.13 and 65.32+/-6.70 micromol/l), compared to the control group (41.24+/-3.65 micromol/l), while group I showed statistically lower values (32.38+/-3.37 micromol/l). In children with the highest level of NO (group II) NOS activity was two-fold higher (1.77+/-0.59 nmol/ml/min; p<0.01) than in controls (0.98+/-0.23 nmol/ml/min). Catalase activity showed a significant increase and SOD activity a significant decrease in all experimental groups, while GPx was not significantly changed. The results show that immune system dysfunction manifested as vasculitis is associated with significant disturbances in the NO system and free radicals scavengers.

Antioxidants↗
PubMed1998

Cell-mediated immunity and postpartum thyroid dysfunction: a possibility for the prediction of disease?

Postpartum (pp) thyroid dysfunction (PPTD) is thought to be caused by an autoimmune (AI) destruction of thyroid follicles during the pp period. The chronic thyroid AI process [already present in pregnancy, as shown by the positivity for thyroid peroxidase antibodies (TPO-Ab)] becomes overt disease in the pp period, and one assumes that this exacerbation represents a rebound phenomenon after a general immunosuppression during pregnancy. The presence of TPO-Ab in pregnancy has been suggested as a predictor for later PPTD development. Apart from B cells, e.g. production of autoantibodies, various functions of the cell-mediated immune (CMI) system, including those of peripheral T cells, monocytes, and dendritic cells (DC), are also disturbed in AI states. The objectives of the present study were: determining alterations in various CMI parameters in pregnancies followed by PPTD vs. those not followed by PPTD; and determining the usefulness of these parameters in the prediction of PPTD. In a prospective study (region: Kempenland, southeast Netherlands), a random sample of 291 women were tested at 12 and 32 weeks gestation and 4 weeks pp for TPO-Ab. Women were followed until 9 months pp, for developing PPTD. PPTD was defined as both: an abnormal TSH, and fT4 pp women developing PPTD and/or being positive for TPO-Ab (n = 26); and thyroidological uneventful control women of the same cohort, matched for age and parity (n = 21), were tested for thyroid-stimulating antibodies, percentages of peripheral blood lymphocyte subsets using fluorescence-activated cell sorter analysis (CD3, CD4, CD8, CD16, CD56, major histocompatibility complex-class II), for monocyte polarization, and for cluster capability of monocyte-derived DC. Results were: 1) 31 women (10.7%) were positive for TPO-Ab (TPO-Ab+) in gestation (12 and/or 32 weeks); 2) 15 women (5.2%) developed PPTD, of whom 10 were TPO-Ab+ in gestation; 3) pregnancy-related CMI alterations consisted of low percentages of CD16+CD56+ natural killer (NK), cells and a low DC cluster capability at 12 weeks gestation (these functions were normalized at 32 weeks gestation); 4) the TPO-Ab+ PPTD+ women (4 hyper, 5 hypo, and 1 hyper/hypo) were characterized by a persistently low percentage of NK cells, a lowered monocyte polarization, and a raised percentage of major histocompatibility complex-class II+CD3+ T cells; 5) the TPO-Ab- PPTD+ women (all 5 hyper) had neither thyroid-stimulating antibodies nor CMI alterations, apart from those normally seen in pregnancy; 6) 21 women were positive for TPO-Ab in pregnancy but did not develop PPTD (they had the same lowered NK cell percentages and monocyte polarization as the TPO-Ab+ PPTD+ cases, but they had normal percentages of activated peripheral T cells and a lower titer of TPO-Ab); 7) determination of the number of NK cells and monocyte polarization hardly contributed to the prediction of PPTD (as compared with TPO-Ab status), because of strong interindividual variation and close association with the presence of TPO-Ab; and 8) combining TPO-Ab assays with testing for activated T cells was the most optimal parameter for the prediction of TPO-Ab+ cases of PPTD in our small test set. We conclude that TPO-Ab+ pregnant women who develop PPTD show several CMI abnormalities other than those seen in normal pregnant women, such as persistently lower percentage of NK cells, a lowered monocyte polarization, and a raised percentage of activated T cells. The latter seems rather specific for the actual PPTD development and is not found in TPO-Ab+ (but PPTD) uncomplicated pregnancies. TPO-Ab- (but PPTD+) women had no signs of CMI abnormalities (apart from those specific for the pregnancy state). Although studied cases are low in number, our data are suggestive for the existence of two forms of PPTD: a TPO-Ab+ (AI) form (two-thirds of patients, classical PPTD pattern); and a TPO-Ab- (non-AI) form (one-third of patients, only hyper). Such assumption implies that, at best, two

Autoantibodies↗
PubMedDate not supplied

Platelet dysfunction associated with immune-mediated thrombocytopenia in dogs.

The effect of antiplatelet antibody on in vitro platelet function was investigated in 15 dogs with immune-mediated thrombocytopenia (ITP). Platelet aggregation was assessed after addition of serum from healthy dogs (n = 5) or dogs with ITP (n = 15) to platelet-rich plasma from a healthy donor dog. The aggregation responses to adenosine diphosphate, thrombin, and collagen/epinephrine were measured as the maximum aggregation observed after 2 minutes. In 13 of 15 dogs with ITP, maximal aggregation was significantly inhibited in response to ADP, thrombin, or collagen/epinephrine. The slope of the aggregation curve was decreased after addition of serum from 9 of 15 patients. A polyclonal rabbit anti-dog platelet antiserum induced inhibition of aggregation with all 3 agonists. Serum from control dogs neither inhibited nor activated platelet aggregation. Aggregation experiments were repeated with all 3 agonists after addition of patient immunoglobulin (Ig)G or IgG from a healthy dog to platelet-rich plasma. The IgG fraction from 9 of 10 dogs with ITP suppressed platelet aggregation. The IgG fraction from polyclonal rabbit anti-dog platelet antiserum inhibited platelet aggregation with all agonists. These results suggest that many canine ITP patients have circulating antibodies that, in addition to causing platelet destruction, may cause platelet dysfunction.

Adenosine Diphosphate↗
PubMed2006

Immune-endocrine host response to endotoxin in major depression.

OBJECTIVE: An impaired hypothalamic-pituitary-adrenocortical (HPA) function is a well-established finding in major depression (MD), but it is still unclear how this dysfunction affects immune responses in this disorder. METHOD: To further examine the relationship between immune and endocrine responses in MD, 0.4ng/kg body weight endotoxin [LPS] or 100mug hCRH were sequentially applied to 12 patients with MD and to 12 age- and gender-matched healthy controls after pre-treatment with 1.5mg dexamethasone (DEX). Immune (TNF-alpha, IL-6, rectal temperature) and endocrine (ACTH, cortisol) parameters were examined as area under the curve (AUC) levels. RESULTS: After pre-treatment with DEX, LPS evoked an immune response in all participants of the study with most immune parameters significantly related to the endotoxin challenge. However, only a marked immune response resulted in an additional endocrine reaction. Subsequently, the quantitative extent of the endocrine reaction was related to the extent of the immune response after DEX/LPS challenge. Pre-LPS AUC levels of cortisol, ACTH and post-LPS levels of IL-6 as well as the post-CRH AUC levels of cortisol and ACTH were related to the depressive symptomatology as measured by the Beck depression inventory (BDI). In depressive patients who showed increased cortisol plasma levels before LPS, the later increase in IL-6 was reduced. CONCLUSIONS: The challenge with DEX/LPS did not reveal major impairments of evoked immune functions in MD. Only the endocrine parameters and the IL-6 response were related to the depressive symptomatology, suggesting a limited interaction between immune and endocrine dysfunctions in MD.

Adrenocorticotropic Hormone↗
PubMed1999

Human parvovirus B19: relevance in internal medicine.

Infection by the human parvovirus B19 can lead to several clinical manifestations which are relevant in internal medicine. These include aplastic crisis in chronic haemolytic anaemias, exanthemathous disease and arthropathy, mainly in women, and chronic anaemia in the immunocompromised host. After initial replication, probably in the respiratory tract, the virus enters its target cells in the bone marrow, erythroid precursor cells, through its receptor, the blood group P antigen. Viral replication in these cells leads to an arrest in erythropoiesis, normally lasting approximately 1 week. In this stage, an aplastic crisis can be produced in all patients under 'erythropoietic stress'. The viraemia disappears as specific antibodies to the virus become detectable in serum, which may give rise to a rash or arthralgia, symptoms that are probably immune-mediated. In immunologically normal individuals the infection is cleared by the humoral immune system within several weeks, whereafter detectable specific IgG confers lifelong immunity to reinfection. In patients with absent or dysfunctional humoral immunity to this virus, however, persistent infection can occur, which results in chronic suppression of erythropoiesis with chronic anaemia. Passive immunization, by means of normal immunoglobulin preparations has been reported to be effective in treating this condition. Diagnosis of parvovirus infection is usually possible by the detection of specific antibodies of IgM class in cases of recent infection. In patients with aplastic crisis and patients with chronic anaemia diagnosis rests upon the detection of parvovirus B19 DNA in serum by polymerase chain reaction. Parvovirus B19 is a ubiquitous virus. By the age of 15, about 50% of individuals have serologic evidence of a past infection, which may present as the common childhood disease erythema infectiosum. At the age of 70, seroprevalence reaches 80 to 100%. A vaccine against this virus is currently being developed.

Adolescent↗
PubMed2001

No evidence of auditory dysfunction in guinea pigs immunized with myelin P0 protein.

Recent data have focused on the peripheral nerve myelin glycoprotein P0 as a putative autoantigen involved in the autoimmune etiology of some cases of Meniere's disease, idiopathic sensorineural hearing loss and sudden deafness. To determine whether antibodies to myelin P0 can alter cochlear function, 13 healthy guinea pigs were immunized with purified porcine myelin P0 while 10 controls were injected with saline water. The animals were then evaluated for evidence of evolving inner ear disease using immunological, electrophysiological and morphological methods. Twenty-six experimental ears were tested weekly with a brainstem auditory evoked potential technique for a period of 4 months and were compared to 20 control ears. Uniformly, all P0-sensitized guinea pigs showed antibodies to myelin protein P0 as evidenced by ELISA. Clinical signs of inflammatory demyelination were not discernible in P0-sensitized guinea pigs and all the animals were qualitatively normal. No significant increase of evoked potential thresholds was found in the P0-sensitized animals when compared to controls (P>0.05). Peak latencies of waves I, II, III, IV and V and inter-peak latencies in P0-sensitized guinea pigs did not significantly differ from those of controls (P>0.05). Histological sections of inner ear and peripheral nerves were free of disease in both groups. These findings indicate that the sole presence of antibodies to myelin P0 in the sera of guinea pigs or patients suspected of having autoimmune inner ear diseases is unlikely to elicit auditory abnormalities and that additional factors are necessary for the pathogenic development of these disorders.

Animals↗
PubMedDate not supplied

[Salmonella septicemia associated with interleukin 12 receptor beta1 (IL-12Rbeta1) deficiency].

OBJECTIVE: To present a case report of a child who developed sepsis by Salmonella enteritidis associated with the diagnosis of primary immunodeficiency. DESCRIPTION: A twenty-one month old boy presenting fever and skin lesions, bilateral pneumonia with pleural effusion and septic shock. Salmonella enteritidis was isolated in blood cultures and pleural fluid. The identification of the bacteria suggested the presence of the MIM syndrome. The diagnosis of IL-12Rbeta1 was confirmed after IL-12 and IFN-gamma levels were measured using patient cells in a culture medium. The results showed absence of IL-12 and the IFN-gamma post stimulation using BCG. COMMENTS: A severe infection by Salmonella enteritidis is strongly suggestive of an immune system dysfunction. Laboratory tests for humoral, cellular and innate immunity were performed. Interleukin 12 receptor beta1 (IL-12 Rbeta1) deficiency was confirmed after specific laboratory evaluation. The use of INF-gamma is recommended in severe cases.

Bacteremia↗