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M Hide

Publications and source records attributed to M Hide.

At least 19 recordsLinked to original sources
PubMed2006

Specific cpb copies within the Leishmania donovani complex: evolutionary interpretations and potential clinical implications in humans.

Leishmania infantum and Leishmania donovani both pertain to the L. (L.) donovani complex and are responsible for visceral leishmaniasis. To explore the L. donovani complex, we focused our study on cysteine protease B (cpb) and especially on 2 cpb copies: cpbE and cpbF. We selected cpb genes because of their phylogenetic interest and host-parasite interaction involvement. Sequencing these 2 copies revealed (i) that cpbE is specific to L. infantum and cpbF is specific to L. donovani and (ii) that these 2 copies are different in length and sequence. Phylogenetic analysis and protein predictions were carried out in order to compare these copies (i) with other trypanosomatid cpb, especially L. mexicana, and (ii) within the L. donovani complex. Our results revealed patterns specific to the L. donovani complex such as the COOH-terminal extension, potential epitopes and N-glycosylation sites. Moreover, phylogenetic analysis revealed different levels of polymorphism between L. infantum and L. donovani and confirmed the ancestral status of the latter. L. infantum has a shorter sequence and a deleted sequence responsible for modifications in protein conformation and catalytic triad. Considering the clinical aspect, L. infantum dermotropic strains appeared more polymorphic than L. infantum viscerotropic strains.

Amino Acid Sequence↗
PubMed2006

Semi-purification of the immunoglobulin E-sweat antigen acting on mast cells and basophils in atopic dermatitis.

BACKGROUND: Sweating aggravates the symptoms of atopic dermatitis (AD). We have recently reported positive skin reactions and histamine release from basophils in response to autologous sweat in patients with AD. OBJECTIVE: To characterize the biochemical and immunological properties of the substance in sweat that evokes histamine release and to study the usability of the basophil-histamine release test with the sweat antigen for AD. METHODS: Sweat collected from healthy volunteers was purified using chromatographies. Serum immunoglobulin (Ig)E of four patients with AD were purified using an affinity-chromatography column with anti-IgE antibodies. The amount of semi-purified sweat antigen (138 ng protein/ml) that induced a half-maximum reaction of basophils of a patient with AD was utilized for the basophil histamine release test. The involvement of specific IgE and high-affinity IgE receptor (FcepsilonRI) in the reactions was examined using basophils of healthy volunteers, a human mast cell line (LAD2), and a rat basophilic leukemia cell line transfected with human alpha-subunit of FcepsilonRI (RBL-48). RESULTS: The semi-purified sweat antigen induced histamine release from the basophils of 47 of 61 (74.6%) patients with AD and four of 46 (8.7%) healthy controls. Both basophils and mast cells sensitized with the patient-derived IgE showed degranulation upon stimulation with the sweat antigen. However, no reaction was observed when cells were sensitized with myeloma IgE or the antigen was treated with proteases. CONCLUSION: The semi-purified standardized sweat antigen consists of a protein that induces degranulation of basophils and mast cells via antigen-specific IgE and FcepsilonRI in patients with AD.

Adolescent↗
PubMed2006

Oral administration of pulverized Konjac glucomannan prevents the increase of plasma immunoglobulin E and immunoglobulin G levels induced by the injection of syngeneic keratinocyte extracts in BALB/c mice.

BACKGROUND: Immunoglobulin (Ig) E plays a key role in the pathogenesis of atopic diseases, such as asthma, atopic dermatitis and allergic rhinitis. Oral administration of pulverized Konjac glucomannan (PKGM) has recently been demonstrated to prevent both plasma IgE elevation and developing dermatitis in NC/Nga mice, a model of atopic dermatitis. OBJECTIVE: To clarify the direct effect of PKGM on the increase of plasma IgE, we employed the system of BALB/c mouse that increases IgE level without developing dermatitis in response to continuous injection of the extract of syngeneic keratinocytes, PAM 212 cells (PAM extract). METHODS: Three weeks after the start of feeding with either control or PKGM diet, mice were injected subcutaneously with PAM extract bi-weekly for 10 weeks. The levels of plasma Igs were measured by enzyme-linked immunosorbent assay every 2 weeks after the injection. The levels of epsilon germline transcription and the amounts of mRNA for IL-4, IFN-gamma, GATA-3 and T bet gene in the spleen were evaluated by real-time RT-PCR at the end of the experiment. RESULTS: On the one hand, PKGM prevented the increase of plasma IgE and IgG (IgG1, IgG2b) induced by PAM extract, and on the other hand, it enhanced the levels of plasma IgG3. However, it did not affect the level of plasma IgM. PKGM also reduced the levels of plasma ovalbumin (OVA)-specific IgE in OVA-sensitized mice. Moreover, PKGM attenuated the induction of epsilon germline transcription and expression levels of mRNA for IL-4, IFN-gamma and GATA-3 in the spleen of PAM extract-injected mice. PKGM also attenuated the induction of epsilon germline transcription and mRNA for IFN-gamma and T bet in the spleen of phosphate-buffered saline-injected control mice. CONCLUSIONS: These results suggested that oral administration of PKGM prevents the elevation of plasma IgE by suppressing IgE class switching in B cells and/or the commitment development of naive lymphocytes to both T-helper type 1 (Th1) and Th2.

Administration, Oral↗
PubMed2005

Prevalence of atopic dermatitis in Japanese elementary schoolchildren.

BACKGROUND: Although there have been several reports on the prevalence of atopic dermatitis (AD) in Japanese schoolchildren based on questionnaires, there has been no nation-wide study of the frequency of this condition diagnosed by dermatologists in regular health check-ups of schoolchildren. OBJECTIVES: The objective of this work was to evaluate precisely the prevalence of AD in elementary schoolchildren in Japan based on regular health check-ups by dermatologists. METHODS: In 2001/2, elementary schoolchildren: first graders (age 6-7 years) and sixth graders (age 11-12 years) were examined by dermatologists in eight prefectures of Japan (Hokkaido, Iwate, Tokyo, Gifu, Osaka, Hiroshima, Kochi and Fukuoka). In each prefecture, public elementary schools were randomly selected from urban and rural districts. We planned to examine about 700 schoolchildren in each of urban first, urban sixth, rural first and rural sixth grades from the eight areas, a total of 22 400 children (700 x 4 x 8). AD was diagnosed by the dermatologists based on the Japanese Dermatological Association criteria for the disease. RESULTS: The point prevalence of AD was 11.2% overall (2664 of 23 719) ranging from 7.4% (Iwate) to 15.0% (Fukuoka) in the eight areas. Seventy-four per cent, 24%, 1.6% and 0.3% of those afflicted were in the mild, moderate, severe and very severe groups, respectively. Overall, the prevalence of first graders was slightly higher than that of sixth graders (11.8% vs. 10.5%, P < 0.01). There was no apparent difference in prevalence between urban and rural districts, or between boys and girls. CONCLUSIONS: The prevalence of AD in Japanese elementary schoolchildren was about 10%, three-quarters of those being mildly affected. This is the first nation-wide study made of Japanese elementary schoolchildren examined by dermatologists to evaluate the frequency of AD.

Child↗
PubMed2005

Molecular cloning of a class IV chitinase allergen from Japanese cedar (Cryptomeria japonica) pollen and competitive inhibition of its immunoglobulin E-binding capacity by latex C-serum.

BACKGROUND: Japanese cedar (Cryptomeria japonica) pollinosis is one of the most prevalent allergic diseases in Japan. Only three C. japonica allergens, Cry j 1, Cry j 2, and CJP-6, have been characterized. The full IgE-binding spectrum of C. japonica pollen allergens demonstrates that many allergens remain to be identified. OBJECTIVE: The aim of this study was to characterize a novel allergen with a high frequency of IgE binding. METHODS: The cDNA coding for a high-frequency IgE-binding protein, designated CJP-4, was cloned from the total mRNA of C. japonica pollen. The corresponding native allergen was purified by affinity precipitation with colloidal chitin and gel chromatography. The IgE-binding ability of purified native CJP-4 was characterized by ELISA and ELISA inhibition. RESULTS: The CJP-4 cDNA encoded 281 amino acids with significant sequence homology to class IV chitinases. Purified native CJP-4, migrated as a homogeneous 34-kDa protein on SDS-PAGE, revealed endochitinase activity on native PAGE. The purified protein displayed the ability to bind IgE from all patients tested (31/31) in ELISA, whereas Cry j 1 bound to IgE at a 71% frequency (22/31). Pre-incubation with latex C-serum completely inhibited the reaction of pooled sera IgE from patients with C. japonica pollinosis and/or latex allergy to purified CJP-4. CONCLUSION: We identified CJP-4 as a novel and fourth C. japonica chitinase allergen with high IgE-binding frequency. The competitive IgE-binding profile between C. japonica chitinase and latex C-serum indicated that C. japonica chitinase should be an important pan-allergen in C. japonica pollen.

Allergens↗
PubMed2005

Exercise and aspirin increase levels of circulating gliadin peptides in patients with wheat-dependent exercise-induced anaphylaxis.

BACKGROUND: Food-dependent exercise-induced anaphylaxis (FDEIA) is an allergic reaction characteristically induced by intense exercise combined with the ingestion of causative food. Recent reports have shown that aspirin intake is a contributing factor in some patients with FDEIA. Wheat is known to be the most frequent causative food, and the IgE-binding epitopes of a major wheat allergen (omega-5 gliadin) in wheat-dependent exercise induced anaphylaxis (WDEIA) have already been clarified. However, the mechanism of eliciting the symptom in WDEIA remains not fully understood. OBJECTIVES: The aim of this study was to examine the relationship of serum gliadin levels and allergic symptoms induced by exercise or aspirin in patients with WDEIA. METHODS: Six patients with a history of recurrent anaphylaxis associated with wheat ingestion were diagnosed as having WDEIA by the provocation test, which included wheat ingestion, exercise, aspirin intake and a combination of these challenges. During the tests, serum levels of gliadins were monitored by gliadin-specific sandwich ELISA. The effects of exercise and aspirin on serum gliadin levels were also investigated in four healthy subjects. RESULTS: Immunoreactive gliadins appeared in the sera of patients during the provocation test with both wheat-exercise and wheat-aspirin challenges in parallel with allergic symptoms. Serum gliadin levels also increased under the two same challenge conditions in the healthy subjects, although they exhibited no allergic symptoms. However, low levels of gliadin were detected in the sera of both patients and healthy subjects when challenged with wheat alone. CONCLUSION: We demonstrated for the first time that blood gliadin levels correlate with clinical symptoms induced by exercise and aspirin in patients with WDEIA. These findings suggest that exercise and aspirin facilitate allergen absorption from the gastrointestinal tract.

Adolescent↗
PubMed2001

The IL-6 family cytokines, interleukin-6, interleukin-11, oncostatin M, and leukemia inhibitory factor, enhance mast cell growth through fibroblast-dependent pathway in mice.

Mast cell hyperplasia is observed in various inflammatory skin diseases. Although the mechanisms involved in the pathogenesis of these conditions remains largely uninvestigated, it is speculated that mediators produced in the lesional skin provide a favorable microenvironment for mast cell growth. Among the proinflammatory mediators, leukemia inhibitory factor (LIF), which shares a receptor component (gp130 subunit) with interleukin-6 (IL-6), has been identified as a mast cell growth-enhancing factor produced by cells of the keratinocyte-derived cell line (KCMH-1). In this study, we investigated the effect of four IL-6 family cytokines, IL-6, IL-11, oncostatin M (OSM) and LIF on mast cell growth in a mast cell/fibroblast co-culture system. When mouse bone marrow-derived cultured mast cells (BMMC) were maintained on a NIH/3T3 fibroblast monolayer, these cytokines induced proliferation of the mast cells, but none of the cytokines had any effect on mast cell proliferation in the absence of fibroblasts. mRNA for gp130 and receptors for the four IL-6 family cytokines were detected in NIH/3T3 fibroblasts by reverse transcriptase-mediated polymerase chain reaction. In contrast, only mRNA for the IL-11 receptor and gp130 were detected in BMMC. Tyrosine phosphorylation of gp130 was observed in NIH/3T3 fibroblasts after stimulation with all the cytokines. Some IL-6 family cytokines enhanced the production of stem cell factor (SCF), a potent mast cell growth factor, from NIH/3T3 fibroblasts, but the amount of SCF produced by NIH/3T3 fibroblasts was not paralleled by the mast cell growth-enhancement induced by the IL-6 family cytokines. When anti-SCF antibody was added with the IL-6 family cytokines in the BMMC/fibroblast coculture system, a significant effect of these cytokines remained, although the growth-enhancing activity was markedly reduced. A similar result was obtained when BMMC were prepared from W/W(V)-mice, which lack functional c-kit, in the BMMC/ fibroblast coculture system. These results suggest that IL-6 family cytokines stimulate mast cell growth by a fibroblast-dependent mechanism, and also suggest the existence of another pathway between BMMC and NIH/3T3 fibroblasts cooperating with the SCF/c-kit pathway. IL-6 family cytokines may thus contribute to mast cell hyperplasia in skin diseases.

3T3 Cells↗
PubMed2001

Genetic heterogeneity and phylogenetic status of Leishmania (Leishmania) infantum zymodeme MON-1: epidemiological implications.

Leishinania (Leishmania) infantum zymodeme MON-1 is responsible for the majority of visceral leishmaniasis cases around the Mediterranean basin, albeit that it causes also cutaneous forms. The MON classification is based on starch gel multilocus enzyme electrophoresis (MLEE) typing. The aim of this work was to explore further the genetic diversity and phytogenetic status of this zymodeme by alternative typing techniques. Fourteen L. (L.) infantum/L. (L.) chagasi stocks identified as MON-1 by MLEE in reference laboratories, 3 L. infantum stocks attributed to other zymodemes (MON-24, MON-29, MON-33) and reference standard stocks belonging to other species (L. (L.) major, L. (L.) tropica and L. (L.) donovani) were characterized by 2 different markers: MLEE on cellulose acetate plates and Random Amplified Polymorphic DNA (RAPD). We have obtained 10 different genotypes with RAPD and 6 different genotypes with MLEE on cellulose acetate plates for the 14 L. infantum/L. chagasi MON-1 stocks studied. MLEE and RAPD data gave quite congruent phylogenetic results: L. infantum zymodeme MON-1 was shown to be polyphyletic and genetically heterogeneous. This work confirms the necessity of using different markers to build up a robust phylogeny. Finally the epidemiological and clinical implications of these results are discussed.

Animals↗
PubMed2001

The release of leukotriene B4 from human skin in response to substance P: evidence for the functional heterogeneity of human skin mast cells among individuals.

Substance P is located in cutaneous nerve fibres and induces wheal and flare responses, accompanied by granulocyte infiltration, upon intradermal injection. Studies with animal skin and rat peritoneal mast cells have suggested that substance P induces the release of histamine and leukotriene B4 (LTB4), a potent chemoattractant for granulocytes, from skin mast cells. However, the release of LTB4 has not been detected from mast cells enzymatically isolated from human skin. In order to investigate the mechanism of granulocyte infiltration induced by substance P in human skin, we studied the release of LTB4 and histamine in response to substance P, and the effect of dexamethasone using human skin obtained from 22 nonallergic individuals. Histamine was released from all skin tissue samples in a dose-dependent manner. However, the amount of LTB4 release, both constitutive and inducible, was variable among skin preparations. Substance P induced a large release of LTB4 from the skin of eight donors (twice to six times that of the spontaneous release), but no or only negligible release from the skin of 14 donors. The amount of constitutive release of LTB4 correlated with the amount of tissue histamine. Dexamethasone selectively abolished the inducible release of LTB4, without an effect on histamine release and the constitutive release of LTB4. These results suggest that substance P induces the release of LTB4 in a certain population of human individuals by a glucocorticosteroid-dependent mechanism, and plays an important role in neurogenic inflammation with granulocyte infiltration.

Adolescent↗
PubMed2001

[A case of cholinergic urticaria with epileptic seizure and abnormalities on electroencephalogram].

We report a 10-year-old boy with cholinergic urticaria associated with epileptic seizure and abnormalities on electroencephalogram. In March 1999, many red wheals developed over the entire body during exercise and at increased body temperature. In April, systemic red wheals developed during exercise. Simultaneously, loss of consciousness was noted for 2 to 3 minutes. After the patient's body was cooled, consciousness improved, and these exanthemas disappeared. In the Department of Dermatology, his illness was diagnosed as cholinergic urticaria. Neurologically, a heat tolerance and mental strain induced cholinergic urticaria, followed by generalized epilepsy(clonic seizure). In addition, electroencephalography revealed high voltage polyspikes and 14 Hz positive spikes. The mechanism involved in cholinergic urticaria associated with epileptic seizure was assumed as follows: sweat-promoting stimuli, such as heat, exercise and tension, stimulate the autonomic center in the diencephalon or brain stem, and excitation in the autonomic center is transmitted to the efferent sympathetic nerve, causing cholinergic urticaria; when the intensity of stimulation is high, the autonomic center exhibits abnormal activities and causes epileptic seizure.

Autonomic Nervous System↗
PubMed2000

Visceral leishmaniasis in a German child who had never entered a known endemic area: case report and review of the literature.

We describe a case of visceral leishmaniasis in a 15-month-old German child. Diagnosis was significantly delayed because the patient had no history of travel to known endemic areas. Congenital or blood transfusion-associated leishmaniasis was ruled out. Possible modes of transmission (including a potential new autochthonous focus of the disease in central Europe) are discussed.

Animals↗
PubMed2000

Substance P induces tumor necrosis factor-alpha release from human skin via mitogen-activated protein kinase.

Substance P plays an important role in neurogenic inflammation with granulocyte infiltration. To investigate cytokines involved in the substance P-induced inflammation and the mechanism of cell activation, we studied the release of TNF (tumor necrosis factor)-alpha and histamine from human skin slices in response to substance P and antigen. Substance P induced the release of histamine and TNF-alpha in a dose-dependent manner at concentrations from 0.8 to 100 microM. PD 098059 (2'-amino-3'-methoxyflavone) selectively inhibited the release of TNF-alpha, but not the release of histamine induced by either substance P or antigen. SB 203580 ([4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-++ +imida zole]) slightly inhibited TNF-alpha release induced by antigen, but not that induced by substance P, and slightly enhanced histamine release induced by either stimulation. The release of TNF-alpha in response to either stimulation was inhibited by 1 nM-1 microM dexamethasone, but histamine release was not affected. These results suggest that substance P, in addition to antigen, induced TNF-alpha release from human skin by a mitogen-activated protein (MAP) kinase, predominantly extracellular signaling-regulated protein kinase (ERK)-dependent, and dexamethasone-sensitive pathway, which is separate from that for histamine release from mast cells.

Adult↗
PubMed1999

Molecular epidemiology and evolutionary genetics of Leischmania parasites.

In order to illustrate the relevance of the concepts and methods of evolutionary genetics in the understanding of the epidemiology of pathogenic agents, we develop in this paper the case of the Leishmania, a genus of parasitic protozoa. An extensive study of various natural populations of Leishmania in different countries (Old and New World) was carried out by using Multilocus Enzyme Electrophoresis (MLEE) and Random Amplified Polymorphic DNA fingerprinting (RAPD) as genetic markers. The data have been interpreted in evolutionary genetic terms. The main benefit of this approach has been to better define the concept of species in the genus Leishmnania, on rigorous phylogenetic bases. As a matter of fact, a sound taxonomical background is a prerequisite for any epidemiological approach. Since the biological concept of species is difficult or impossible to apply for most pathogenic microorganisms, we recommend relying on criteria of both phylogenetic discreteness and of epidemiological/medical relevance to describe new species of Leishmania. Through this approach, for example, we have shown that the species status of L. ( V.) perzzl.ianza can be supported. On the contrary, we have been unable to clearly distinguish L. (V.) panamensis from L. (V.) guyanensis with genetic tools. Additionally, we have shown that the epidemiological inferences based on a limited set of genetic markers can be misleading. As a matter of fact, we have demonstrated that a collection of L. (L.) infantum stocks identified as zymodeme 'MON 1' by other authors present additional genetic heterogeneity and do not correspond to a distinct 'Discrete Typing Unit' DTU, and are actually polyphyletic. Lastly, in the samples that were conveniently designed, we have confirmed that Leishmania parasites have a basically clonal population structure. As the clonal model specifies it, occasional bouts of genetic exchange remain nevertheless possible. Telling comparisons are drawn with the evolutionary genetics of other pathogens Trypanosoma cruzi and Trypanosoma congolense.

Animals↗
PubMed1999

Chemical mediators in atopic dermatitis: involvement of leukotriene B4 released by a type I allergic reaction in the pathogenesis of atopic dermatitis.

BACKGROUND: The mediators produced from a type I allergic reaction have not yet been able to explain the pathogenesis of atopic dermatitis (AD). OBJECTIVE: The purpose of this study was to elucidate the involvement of leukotriene (LT) B4 produced from a type I allergic reaction in the pathogenesis of AD. METHOD: The release of LTB4 was measured both in vitro, in passively sensitized and antigen-challenged human skin slices, as well as in vivo, in skin chambers on patients with AD. RESULTS: LTB4 was released from in vitro human skin by stimulation of the antigen (54.9 +/- 14.6 pg/g wet weight of skin by antigen challenge and 28.0 +/- 11.1 pg/g in control skin, P <.002). Antigen-specific release of LTB4 and histamine was also observed in vivo in nonlesional skin from the patients with AD by using the skin chamber technique. CONCLUSION: LTB4 release during type I allergic reaction in human skin has been determined in vitro. The released LTB4 possibly contributes to cellular response at the acute inflammatory lesion of AD.

Adolescent↗
PubMed1999

An assessment of the role of Candida albicans antigen in atopic dermatitis.

An immediate hypersensitivity reaction to Candida albicans (C. albicans) antigen has been observed in patients with atopic dermatitis. Recent data from a comparative study of the immune response to C. albicans antigen in patients with atopic dermatitis and non-atopics suggest a shift form type 1 helper T cells to type 2 helper T cells in the immune response to C. albicans antigen in atopic dermatitis. To delineate the role of C. albicans in the pathogenesis in atopic dermatitis, we evaluated skin reaction of C. albicans antigen, as well as the serum IgE antibody level against C. albicans in patients with atopic dermatitis, patients with nasal allergy, and non-atopics. In addition, the clinical effect of antifungal drugs was evaluated in the patients with atopic dermatitis. As a result, we found that immediate hypersensitivity to C. albicans antigen is strongly correlated with the patients with atopic dermatitis. On the other hand, the delayed-type hypersensitivity to this antigen, which is highly prevalent in atopics without dermatitis as well as non-atopics, was reduced in most of these patients. Antifungal drugs markedly improved the skin manifestations in patients with atopic dermatitis that have IgE antibodies against C. albicans, and the serum IgE levels also decreased. These results suggest that C. albicans antigen is a potent intrinsic factor in inducing skin lesions in atopic dermatitis because of IgE-mediated hypersensitivity of C. albicans antigen.

Adolescent↗
PubMed1998

Histamine enhances UVB-induced IL-6 production by human keratinocytes.

Histamine, an important mediator in immediate-type hypersensitivity, is elevated in the skin of patients with atopic dermatitis and is considered to play a pathogenic role in atopic dermatitis. In this study, to elucidate the mechanism of sun exposure-induced exacerbation of skin lesions in atopic dermatitis, we examined the effect of histamine on proinflammatory cytokine production of keratinocytes induced by ultraviolet (UV) B irradiation. Cultured human keratinocytes were irradiated with 30 mJ/cm2 of UVB and incubated with histamine over the concentration range 10(-7) to 10(-4) M, and the IL-1alpha and IL-6 released into the medium were measured using an ELISA. Histamine weakly stimulated IL-6 production by itself. However, together with UVB, it synergistically enhanced IL-6 production and the amount of IL-6 mRNA as estimated by reverse-transcription polymerase chain reaction (RT-PCR). Histamine had a dose-dependent effect which was maximal at a concentration of 10(-5) M, and had no effect on the kinetics of IL-6 production. In contrast, histamine had no effect on IL-1alpha production by keratinocytes. The effect of histamine was completely blocked by pyrilamine, an H1 receptor antagonist, and mimicked by the H1 receptor agonist, 2-methylhistamine. Whereas the H2 receptor antagonist, cimetidine, slightly inhibited the effect of histamine and the effect of the H2 receptor agonist, 4-methylhistamine, was minute. These results show that histamine augments UVB-induced IL-6 production by keratinocytes predominantly via the H1 receptor at the level of transcription. This suggests a contributory role for histamine in the exacerbation of atopic dermatitis induced by sun exposure.

Adult↗