The Experts below are selected from a list of 177 Experts worldwide ranked by ideXlab platform
J P Auffray - One of the best experts on this subject based on the ideXlab platform.
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mimivirus in pneumonia patients
Emerging Infectious Diseases, 2005Co-Authors: Bernard La Scola, Thomas J. Marrie, J P AuffrayAbstract:Mimivirus, the largest virus known to date, is an amebal pathogen like Legionella spp. When mimivirus was used as an antigen in a Migration Inhibition factor assay, seroconversion was found in patients with both community- and hospital-acquired pneumonia. Mimivirus DNA was found in respiratory samples of patients with hospital-acquired pneumonia.
Bernard La Scola - One of the best experts on this subject based on the ideXlab platform.
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mimivirus in pneumonia patients
Emerging Infectious Diseases, 2005Co-Authors: Bernard La Scola, Thomas J. Marrie, J P AuffrayAbstract:Mimivirus, the largest virus known to date, is an amebal pathogen like Legionella spp. When mimivirus was used as an antigen in a Migration Inhibition factor assay, seroconversion was found in patients with both community- and hospital-acquired pneumonia. Mimivirus DNA was found in respiratory samples of patients with hospital-acquired pneumonia.
Thomas J. Marrie - One of the best experts on this subject based on the ideXlab platform.
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mimivirus in pneumonia patients
Emerging Infectious Diseases, 2005Co-Authors: Bernard La Scola, Thomas J. Marrie, J P AuffrayAbstract:Mimivirus, the largest virus known to date, is an amebal pathogen like Legionella spp. When mimivirus was used as an antigen in a Migration Inhibition factor assay, seroconversion was found in patients with both community- and hospital-acquired pneumonia. Mimivirus DNA was found in respiratory samples of patients with hospital-acquired pneumonia.
Sima Halevy - One of the best experts on this subject based on the ideXlab platform.
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in vitro release of interferon gamma and macrophage Migration Inhibition factor in drug induced urticaria and angioedema
Acta Dermato-venereologica, 1999Co-Authors: Ella Livni, Moshe Lapidoth, Sima HalevyAbstract:: T-cells are involved in the pathogenesis of cutaneous drug reactions. T-cell phenotype and cytokine release pattern in rivo and in vitro might correlate with the type of immune response involved in cutaneous drug reactions. In vitro release of interferon-gamma and macrophage Migration Inhibition factor (MIF) from peripheral blood lymphocytes, following in vitro challenge with the suspected unmodified drugs, was studied in 12 patients with drug-induced urticaria and/or angioedema and in two group-matched controls. The occurrence of positive interferon-gamma and MIF responses was significantly higher in patients with drug-induced urticaria and/or angioedema than in controls. The sensitivity and specificity of the interferon-gamma test (50% and 92%, respectively) were similar to that of the MIF test (58% and 96%, respectively). Percentage agreement between both tests was 80.9 (kappa = 0.76). In vitro release of interferon-gamma and MIF in drug-induced urticaria and/or angioedema suggests a drug-specific immune response, and may implicate the drug as a possible inducer of the reaction.
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the role of macrophage Migration Inhibition factor in toxic epidermal necrolysis
International Journal of Dermatology, 1997Co-Authors: Sima Halevy, Ella LivniAbstract:Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A macrophage Migration Inhibition factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The macrophage Migration Inhibition factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P<0.05) than that recorded in the controls (0/17). The MIF test results in TEN patients and controls are summarized in Table 1.
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allergic vasculitis induced by decapeptyl confirmation by macrophage Migration Inhibition factor mif test
European Journal of Obstetrics & Gynecology and Reproductive Biology, 1993Co-Authors: Boaz Amichai, Marcelo H Grunwald, Sima HalevyAbstract:Abstract A case of allergic vasculitis of the skin following treatment with Decapeptyl ® ( d -Trp 6 -LHRH) for in vitro fertilization is described. The possible role of an allergic mechanism in this reaction has been suggested by a positive macrophage Migration Inhibition factor (MIF) test toward the drug.
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macrophage Migration Inhibition factor release in lichenoid drug eruptions
Journal of The American Academy of Dermatology, 1993Co-Authors: Sima Halevy, Miriam Sandbank, Ella LivniAbstract:Lichenoid drug eruption (DE) that can clinically and histologically resemble lichen planus (LP) can be induced by gold, thiazide diuretics, quinidine, and other agents. 1, 2 Lichenoid DE, which in general spares the mucous membranes, may be photodistributed or nonphotodistributed.P Common causes of photodistributed lichenoid DE are thiazide diuretics-" and quinidine.': 5 The mechanism by which drugs induce a lichenoid tissue reaction is unknown. Recent observations support a critical role of helper/inducer T lymphocytes in lichenoid tissue reaction." In isolated cases of lichenoid photosensitive DE induced by hydrochlorothiazide or quinidine, positive macrophage Migration Inhibition factor (MIF) responses toward the offending drugs were recorded.f5 MIF is a lymphokine released from sensitized T lymphocytes by an appropriate antigen. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in animal models and in humans.71O Furthermore, MIF release has been recently reported to be valuable in the diagnosis of adverse drug reactions, including DE,ll-15 The present study was conducted to evaluate MIF release in patients with lichenoid DE induced by various drugs.
Rainer Haas - One of the best experts on this subject based on the ideXlab platform.
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helicobacter pylori interferes with leukocyte Migration via the outer membrane protein hopq and via caga translocation
International Journal of Medical Microbiology, 2015Co-Authors: Benjamin Busch, Ramona Weimer, Christine Woischke, Wolfgang Fischer, Rainer HaasAbstract:The human gastric pathogen Helicobacter pylori is a paradigm for chronic bacterial infections. Persistent colonization of the stomach mucosa is facilitated by several mechanisms of immune evasion and immune modulation, such as avoidance of Toll-like receptor recognition or skewing of effector T cell responses. Interactions of H. pylori with different immune cells have been described with respect to immune cell activation, cytokine release, or oxidative burst induction. We show here that H. pylori infection of human granulocytes, or of HL-60 cells differentiated to a granulocyte-like phenotype (dHL-60 cells) results in Inhibition of cell Migration under different conditions. Migration of dHL-60 cells in a three-dimensional collagen gel was found to be inhibited independently of the cag pathogenicity island, whereas Migration Inhibition in an under agarose assay was dependent on the cag pathogenicity island, on its effector protein CagA, and on the outer membrane protein HopQ. CagA translocation into leukocytes is accompanied by its tyrosine phosphorylation and by proteolytic processing into an N-terminal 100 kDa and a C-terminal 35 kDa fragment at a distinct cleavage site. By using complemented H. pylori strains producing either phosphorylation-resistant or cleavage-resistant CagA variants, we show that CagA tyrosine phosphorylation is required for Migration Inhibition, but CagA processing is not. Our results suggest that direct contact of H. pylori with immune cells subverts not only their activation characteristics, but also their migratory behaviour.