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51.
A. L. Van Gasse V. Sabato A. P. Uyttebroek J. Elst M. A. Faber M. M. Hagendorens C. Mertens C. H. Bridts L. S. De Clerck D. G. Ebo 《Allergy》2017,72(12):2039-2043
Immediate drug hypersensitivity reactions (IDHR) to moxifloxacin constitute a pathomechanistic conundrum and a diagnostic challenge. Our objective was to study whether simultaneous phenotyping and quantification of histamine release might add to our knowledge about the basophil activation properties of moxifloxacin and constitute a reliable diagnostic aid. Fifteen patients with an IDHR to moxifloxacin and nine moxifloxacin challenged controls were selected. All had a basophil activation test (BAT) with moxifloxacin. Flow cytometric analysis of basophil responses implied labeling for CD63, CD203c, and intracellular histamine. Unlike tolerant challenged controls, basophilic upregulation of CD203c in response to moxifloxacin was observed in seven of 15 patients. Only two of these seven patients demonstrated appearance of CD63 and release of histamine. In the remainder eight patients, no basophil responses were demonstrable. In conclusion, immediate hypersensitivity to moxifloxacin might involve mechanisms difficult to capture by traditional CD63‐/CD203c‐based BAT. Deciphering the complexity of quinolone IDHR seems mandatory. 相似文献
52.
The clinical utility of basophil activation testing in diagnosis and monitoring of allergic disease
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H. J. Hoffmann A. F. Santos C. Mayorga A. Nopp B. Eberlein M. Ferrer P. Rouzaire D. G. Ebo V. Sabato M. L. Sanz T. Pecaric‐Petkovic S. U. Patil O. V. Hausmann W. G. Shreffler P. Korosec E. F. Knol 《Allergy》2015,70(11):1393-1405
The basophil activation test (BAT) has become a pervasive test for allergic response through the development of flow cytometry, discovery of activation markers such as CD63 and unique markers identifying basophil granulocytes. Basophil activation test measures basophil response to allergen cross‐linking IgE on between 150 and 2000 basophil granulocytes in <0.1 ml fresh blood. Dichotomous activation is assessed as the fraction of reacting basophils. In addition to clinical history, skin prick test, and specific IgE determination, BAT can be a part of the diagnostic evaluation of patients with food‐, insect venom‐, and drug allergy and chronic urticaria. It may be helpful in determining the clinically relevant allergen. Basophil sensitivity may be used to monitor patients on allergen immunotherapy, anti‐IgE treatment or in the natural resolution of allergy. Basophil activation test may use fewer resources and be more reproducible than challenge testing. As it is less stressful for the patient and avoids severe allergic reactions, BAT ought to precede challenge testing. An important next step is to standardize BAT and make it available in diagnostic laboratories. The nature of basophil activation as an ex vivo challenge makes it a multifaceted and promising tool for the allergist. In this EAACI task force position paper, we provide an overview of the practical and technical details as well as the clinical utility of BAT in diagnosis and management of allergic diseases. 相似文献
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Monocyte-mediated antibody-dependent cell-mediated cytotoxicity: the role of the metabolic burst 总被引:4,自引:0,他引:4
Human monocytes respond to opsonized microorganisms with a "metabolic burst" composed of an increase in oxygen consumption, an increase in hexose monophosphate shunt (HMPS) activity, and the generation of reactive oxygen species (ROS). We investigated the role of the metabolic burst in antibody-dependent cell-mediated cytotoxicity (ADCC) by human monocytes toward anti-D coated erythrocyte target cells because recent studies suggested a role for oxygen-dependent bactericidal mechanisms in ADCC. In normal monocytes, we found that ADCC was nearly halved under hypoxic conditions. Several agents known to impair activation of the burst, such as vincristine, cation chelators, and a sulfhydryl reagent, all decreased cytotoxicity if added before initiation of contact between target and effector cells. Cytotoxicity was inhibited by 2-deoxyglucose but not fluoride, suggesting a nonglycolytic role for glucose in ADCC, perhaps in the HMPS pathway. Although these data suggested a role for the metabolic burst in ADCC, scavengers of ROS did not impair cytotoxicity, and monocytes from chronic granulomatous disease (CGD) patients who had a defective metabolic burst had normal levels of ADCC. We conclude that ADCC toward anti-D coated erythrocyte target cells was the result of at least two independent but closely related cytotoxic pathways. Although one of these pathways appeared to involve the metabolic burst, the potentially cytotoxic reactive oxygen species did not appear to play a role in this system. 相似文献
55.
56.
Lopez AF; Dyson PG; To LB; Elliott MJ; Milton SE; Russell JA; Juttner CA; Yang YC; Clark SC; Vadas MA 《Blood》1988,72(5):1797-1804
Recombinant human (rh) interleukin-3 (IL-3) stimulated the proliferation and differentiation of erythroid, granulocyte, macrophage, eosinophil (Eo), and mixed colonies as well as megakaryocytes from human bone marrow cells. rh IL-3 was a weaker stimulus than rh granulocyte-macrophage colony-stimulating factor (GM- CSF) for day 14 myeloid cell colonies. At day 7 of incubation, rh IL-3 stimulated a few G, M, and Eo clusters but no colonies. This loss of responsiveness of myeloid cells to rh IL-3 was accentuated with further differentiation of the cells. rh IL-3 stimulated very few or no clones after five-day incubation with enriched promyelocytes and myelocytes, whereas rh GM-CSF was an efficient stimulus. Responsiveness to rh IL-3 was completely lost in postmitotic mature neutrophils. Incubation of these cells with rh IL-3 did not result in enhanced antibody-dependent cell-mediated cytotoxicity (ADCC) of tumor cells or superoxide anion production after stimulation with formyl-methyl-leucyl-phenylalanine (FMLP), although they could be stimulated by rh GM-CSF. In addition, preincubation of neutrophils with different concentrations of rh IL-3 failed to increase or decrease their response to rh GM-CSF. In contrast to neutrophils, mature Eos could be stimulated by rh IL-3 to kill antibody-coated tumor cells. These results show that cells of the neutrophilic myeloid series lose their responsiveness to h IL-3 as they differentiate and suggest that although h IL-3 may be an important therapeutic agent to use for hematopoietic regeneration in vivo, the lack of stimulation of mature neutrophil function makes it an unlikely sole candidate as adjunct therapy for treatment of infectious diseases. 相似文献
57.
Deletions of the cyclin-dependent kinase inhibitor genes p16INK4A and p15INK4B in non-Hodgkin's lymphomas 总被引:7,自引:0,他引:7
The tumor suppressor genes p16INK4A and p15INK4B map to the 9p21 chromosomal locus and are either homozygously deleted or mutated in a wide range of human cancer cell lines and tumors. Although chromosome 9 abnormalities have been described in non-Hodgkin's lymphomas (NHLs), to date, the mutational status of these genes has not been determined for these malignancies. A total of five cell lines and 75 NHLs were examined for homozygous deletions or point mutations in the coding regions of both the p15 and p16 genes using Southern blot and/or polymerase chain reaction-single-strand conformation polymorphism analyses. Homozygous deletions of either the p16 gene or both the p15 and p16 genes were observed in one diffuse large B-cell lymphoma cell line and two uncultured lymphomas consisting of one large B-cell and one mixed T-cell lymphoma. In contrast, point mutations were not detected in either the cell lines or lymphomas. These results indicate that the rate of alterations in the p15 and p16 genes is low for lymphomas, but loss of p16 and/or p15 may be involved in the development of some lymphomas. 相似文献
58.
Paul Guedeney Sabato Sorrentino Birgit Vogel Usman Baber Bimmer E. Claessen 《Expert review of cardiovascular therapy》2013,11(11):825-835
ABSTRACTIntroduction: Chronic kidney disease (CKD) is commonly present in patients undergoing percutaneous coronary intervention (PCI). These patients frequently present with more complex coronary artery disease (CAD) and higher risk of peri-procedural and post-procedural adverse events, including bleeding, thrombotic events, and contrast-induced acute kidney injury (CI-AKI). This article contains updated knowledge and management of patients with CKD undergoing PCI.Areas covered: In this article, the pathophysiological mechanisms behind the association of CKD, complex CAD lesions, and complications of PCI are reviewed and the different risk scores available to assess the occurrence of CI-AKI are detailed. Furthermore, various strategies developed to prevent or reduce the impact of complications of PCI are described.Expert commentary: Patients with CKD have remained a challenge in the field of PCI. Several strategies have been evaluated in the last 20 years, with uneven results. Intravascular expansion therapy remains the cornerstone of CI-AKI prevention although recent studies have emphasized the benefit of guided hydration rather than a one-size-fits-all model. N-acetylcysteine and sodium bicarbonate have recently been challenged while pretreatment with high-dose statins may be of interest. Finally, recent studies based on intravascular ultrasound and minimal-to-no-use of contrast media have yielded promising results. 相似文献
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60.
Taneli Puumalainen Beatriz Quiambao Erma Abucejo-Ladesma Socorro Lupisan Tarja Heiskanen-Kosma Petri Ruutu Marilla G Lucero Hanna Nohynek Eric AF Simoes Ian Riley 《BMC infectious diseases》2008,8(1):1-7