Reliability of IFCC method for lactate dehydrogenase measurement in lithium-heparin plasma samples.
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Anticoagulants↗
Biomedical subjects
Harald Renz
Publications and source records attributed to Harald Renz.
Environmental exposure to endotoxin and its relation to asthma in school-age children.
BACKGROUND: In early life, the innate immune system can recognize both viable and nonviable parts of microorganisms. Immune activation may direct the immune response, thus conferring tolerance to allergens such as animal dander or tree and grass pollen. METHODS: Parents of children who were 6 to 13 years of age and were living in rural areas of Germany, Austria, or Switzerland where there were both farming and nonfarming households completed a standardized questionnaire on asthma and hay fever. Blood samples were obtained from the children and tested for atopic sensitization; peripheral-blood leukocytes were also harvested from the samples for testing. The levels of endotoxin in the bedding used by these children were examined in relation to clinical findings and to the cytokine-production profiles of peripheral-blood leukocytes that had been stimulated with lipopolysaccharide and staphylococcal enterotoxin B. Complete data were available for 812 children. RESULTS: Endotoxin levels in samples of dust from the child's mattress were inversely related to the occurrence of hay fever, atopic asthma, and atopic sensitization. Nonatopic wheeze was not significantly associated with the endotoxin level. Cytokine production by leukocytes (production of tumor necrosis factor alpha, interferon-gamma, interleukin-10, and interleukin-12) was inversely related to the endotoxin level in the bedding, indicating a marked down-regulation of immune responses in exposed children. CONCLUSIONS: A subject's environmental exposure to endotoxin may have a crucial role in the development of tolerance to ubiquitous allergens found in natural environments.
Adolescent↗
Augmentation of allergic early-phase reaction by nerve growth factor.
The allergic early-phase reaction, a hallmark of allergic bronchial asthma, is caused by allergen and immunoglobulin E-dependent mediator release from mast cells. It was previously shown that nerve growth factor (NGF) contributes to acute airway inflammation. This study further investigates the role of NGF in the allergic early-phase reaction using a well-established mouse model of ovalbumin-induced allergic airway inflammation. Treatment of sensitized and aerosol challenged BALB/c mice with blocking anti-NGF antibodies inhibited allergen-induced early-phase reaction and suppressed airway inflammation. Transgenic mice constitutively overexpressing NGF in the airways (Clara-cell secretory protein promoter [CCSP]-NGF-tg) were employed and compared with wild-type animals. In sensitized and challenged CCSP-NGF-tg mice, early-phase reaction, airway inflammation, as well as percental relative increases in serotonin levels were augmented compared with wild-type mice. These effects were paralleled by increased serotonin levels in the airways, whereas immunoglobulin E levels remained unaffected. Furthermore, CCSP-NGF-tg mice developed an increased reactivity of sensory neurons in response to inhaled capsaicin demonstrating NGF-mediated neuronal plasticity. These data provide evidence for the functional role of NGF in the development of allergic early phase responses in the airways and the lung.
Acute-Phase Reaction↗
[Immunotherapy in broad allergy spectrum].
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Adolescent↗
Diagnostic value of peripheral blood T-cell activation and soluble IL-2 receptor for acute rejection in liver transplantation.
BACKGROUND: T-cells play an important role in the pathogenesis of rejection. Monitoring T-cells activation markers in peripheral blood may contribute to diagnosis of acute rejection after liver transplantation (LTX). METHODS: Lymphocyte subset distribution, expression of T-cell activation markers (flow cytometry), concentration of soluble (s) interleukin-2 receptor (IL-2R) (solid phase chemiluminescence immunoassay), and liver enzymes as well as bilirubin were prospectively tested in peripheral blood samples of LTX patients with (n=69) and without acute rejection (n=50). Acute rejection was assessed by standard criteria including liver biopsies. RESULTS: Intra-individual monitoring of immune parameters revealed an up-regulation of IL-2 receptor (CD25) expression on CD4 and CD8 T-cells together with increases in sIL-2R levels in patients with acute rejections. Measuring sIL-2R levels resulted in highest diagnostic efficiency (>85%). This level of diagnostic efficiency was not reached by any other marker tested. From all conventional markers of hepatocellular integrity and function, alkaline phosphatase reached the highest level of diagnostic efficiency with 70%. CONCLUSIONS: Monitoring of up-regulation of the IL-2/IL-2R pathway represents a useful tool for assessment of acute rejection after LTX.
Acute Disease↗
Control of nerve growth and plasticity.
Respiratory function is under close control of the autonomic nervous system. Recent data indicate that dysfunction and dysregulation of both the non-adrenergic non-cholinergic (NANC) and cholinergic system contribute to the pathogenesis of chronic inflammatory lung disease such as bronchial asthma. Sensory neurons of the NANC system in particular exhibit a great degree of plasticity. It has been shown that neurotrophins play an important role in modulating sensory innervation in such conditions. In addition, several inflammatory mediators also contribute to sensory nerve plasticity in this context. Cholinergic nerves represent the dominant broncho-constrictory pathway and the role of the muscarinic M(2) receptor has been recently characterized in this regard. In summary, recent data provide new insights into dysfunction and dysregulation of the autonomic nervous system as observed in chronic inflammatory lung disease.
Animals↗
T(H)1/T(H)2 immune response profiles differ between atopic children in eastern and western Germany.
BACKGROUND: Lower prevalence rates for childhood respiratory allergies have been reported in eastern Germany than in western Germany. OBJECTIVE: Because allergic phenotypes are thought to be associated with an unbalanced T(H)1/T(H)2 T cell effector response, a cross-sectional investigation was carried out as part of the German ISAAC Phase II study to determine whether T(H)1/T(H)2 capacity might have developed in different directions during the separation between the 2 parts of the country. METHODS: In a community-based random sample of 9- to 11-year-old (n = 6399) and 5- to 7-year-old (n = 6202) children in eastern and western Germany, the prevalence of atopy was assessed. Heparinized blood samples were collected from a subgroup of children stratified according to the number of older siblings. T(H)1 and T(H)2 cytokine productivity was determined after stimulation with phorbol ester plus ionomycin. RESULTS: Individuals who grew up in eastern Germany had a marked bias toward T(H)0 responsiveness (>60%), regardless of whether they were atopic. In contrast, the children of western Germany, particularly when they were atopic, showed T(H)2 polarization. CONCLUSIONS: This is the first epidemiologic survey to demonstrate regional differences in the T(H)1/T(H)2 response pattern and their relation to atopic disease between regions.
Asthma↗
Vbeta18.1(+) and V(alpha)2.3(+) T-cell subsets are associated with house dust mite allergy in human subjects.
BACKGROUND: The recognition of allergenic peptides by T cells through their T-cell receptor (TCR) represents a crucial step in the initiation of an allergen-specific immune response. In parallel to the superantigen-driven restricted expansion of Vbeta subsets in autoimmune and infectious diseases, reports in animals and human subjects have shown a similar capacity of classical antigens. OBJECTIVE: The study was performed to analyze the V(alpha)/Vbeta expression in house dust mite (HDM) allergy. METHODS: The TCR repertoire of 15 subjects with HDM allergy, 22 atopic subjects without HDM allergy, and 19 nonatopic individuals, members of 2 extended and 4 nuclear families, was determined. By using flow cytometry, the expression of 22 Vbeta and 3 V(alpha) elements was analyzed in vivo and after in vitro allergen stimulation. RESULTS: In comparison with nonatopic and atopic individuals without HDM allergy, freshly isolated PBMCs of individuals with HDM allergy showed a significantly higher frequency of Vbeta18(+) and V(alpha)2.3(+) T cells. Although members of all 3 groups had a similar lymphocyte proliferation response after in vitro stimulation with Der p 1 or Der p 1 peptide(101-131), a significant expansion of Vbeta18(+) and V(alpha)2.3(+) T cells in vitro occurred only in individuals with HDM allergy. Moreover, the degree of expansion correlated with the levels of allergen-specific IgE antibodies. No expansion of Vbeta18(+) and V(alpha)2.3(+) was observed after mitogen stimulation with PHA, indicating allergen specificity of the response. CONCLUSION: Our results strongly suggest restricted TCR V(alpha)/Vbeta gene use in HDM allergy and might be a step toward TCR-based immunotherapy.
Adolescent↗
Unusual late onset of X-linked chronic granulomatous disease in an adult woman after unsuspicious childhood.
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Adult↗
Stress enhances airway reactivity and airway inflammation in an animal model of allergic bronchial asthma.
OBJECTIVE: Despite the long-standing clinical assumption that stress and asthma morbidity are associated, convincing experimental evidence on mechanisms has been unavailable. A wide range of immunological, endocrinological, and neuronal pathways are known to mediate and modulate a systemic stress response. Interestingly, most of these mediators play a crucial role in initiating and perpetuating symptoms associated with bronchial asthma. To explore potential mechanisms linking stress to asthma exacerbation we developed an animal model that combines allergic airway inflammation and exposure to stress. METHODS: CBA/J mice were sensitized by intraperitoneal injection of ovalbumin (OVA) and challenged with OVA aerosol via the airways. Additionally, some mice were stressed by exposure to an ultrasonic stressor. Airway hyperreactivity (AHR) was measured in vitro by electric field stimulation (EFS) of tracheal smooth muscle elements. Bronchoalveolar lavage fluid (BAL) was obtained and cell numbers determined. Cytokine levels of IL-4, IL-5, and IFN-gamma in BAL were determined by ELISA. RESULTS: Our findings demonstrate that exogenously applied stress dramatically enhances airway reactivity in OVA-sensitized and challenged mice. Further, stress significantly increases allergen-induced airway inflammation identified by increased leukocyte (ie, eosinophil) numbers in bronchoalveolar lavage fluids. CONCLUSIONS: We found further evidence that stress can indeed exacerbate airway hyperreactivity and airway inflammation in an animal model of allergic bronchial asthma and now introduce a novel murine model to identify stress-triggered pathways, including mediators as neurohormones, neuropeptides, and markers of inflammation.
Aerosols↗