Aminophilline suppress the release of chemical mediators in treatment of acute asthma.

Background: The control of airway inflammation is crucial for management of asthma. Theophylline has been demonstrated to have an anti-inflammatory effect as a long-term-medication for asthma in various studies. In the present study we attempted to clarify if aminophylline, a theophylline derivative, could act as an anti-inflammatory agent as well as a bronchodilator in the treatment for acute asthma exacerbations.

Association of transforming growth factor-beta1 single nucleotide polymorphism C-509T with allergy and immunological activities.

Background: A single nucleotide polymorphism (SNP) C-509T within the tumor growth factor beta1 (TGFbeta1) gene has been associated with atopic asthma and asthma severity. To further understand the mechanisms involved, the association of C-509T with allergy, T-lymphocyte proliferation and plasma TGFbeta1 concentration has been explored in a case-control study with allergic and non-allergic subjects.

Methods: The recruited subjects including allergic (n = 38) and nonallergic (n = 25) participants have been genotyped for C-509T using allele discrimination assay.

Role of insulin-like growth factor-I in allergen-induced airway inflammation and remodeling.

Insulin-like growth factor (IGF)-I is known to act on fibroblasts as a progression factor to push cells toward proliferation and activation to synthesize collagen. Subepithelial fibrosis, collagen deposition at the lamina reticularis, is part of the process of so-called remodeling and is a characteristic finding in the asthmatic airway. To study the role of IGF in the evolution of asthma, we used a model that involved immunization of mice with ovalbumin and alum, followed by an inhaled challenge of ovalbumin.

IgE- and FcepsilonRI-mediated migration of human basophils.

Local accumulation of basophils at inflammatory sites is observed in experimental antigen challenge and in allergic diseases. It is not fully known what factor(s) regulates local basophil influx in tissues, and it has not been determined whether antigens belong in a panel of basophil chemoattractants. This study was designed to elucidate whether IgE- and high-affinity receptor for IgE (FcepsilonRI)-mediated stimulation can induce human basophil migration.

A prospective clinical study of theophylline safety in 3810 elderly with asthma or COPD.

A large-scale prospective study was conducted in 3810 Japanese elderly (> or =65 years old) patients with asthma or chronic obstructive pulmonary disease (COPD) who had been treated with sustained-release theophylline tablets (THEODUR) at a dose of 400 mg/day for 1-6 months, in principle. Among 3798 protocol-complying patients (mean age: 73.8 +/- 0.

Transendothelial migration of human basophils.

During allergic reactions, basophils migrate from the blood compartment to inflammatory sites, where they act as effector cells in concert with eosinophils. Because transendothelial migration (TEM) represents an essential step for extravasation of cells, for the first time we have studied basophil TEM using HUVEC. Treatment of HUVEC with IL-1beta significantly enhanced basophil TEM, which was further potentiated by the presence of a CCR3-specific ligand, eotaxin/CCL11.

Optimal trajectory formation of constrained human arm reaching movements.

Opening a door, turning a steering wheel, and rotating a coffee mill are typical examples of human movements that are constrained by the physical environment. The constraints decrease the mobility of the human arm and lead to redundancy in the distribution of actuator forces (either joint torques or muscle forces). Due to this actuator redundancy, there is an infinite number of ways to form a specific arm trajectory.

Activation of epidermal growth factor receptor via CCR3 in bronchial epithelial cells.

We have previously found that bronchial epithelial cells express CCR3 whose signaling elicits mitogen-activated protein (MAP) kinase activation and cytokine production. Several investigators have focused on the signaling crosstalk between G protein-coupled receptors (GPCRs) and epidermal growth factor receptor (EGFR) in cancer cells. In this study, we investigated the role of EGFR in CCR3 signaling in the bronchial epithelial cell line NCI-H292.

Lack of association of CCR4 single nucleotide polymorphism with atopic dermatitis in Japanese patients.

CCR4, a member of the CC chemokine receptor family, is believed to play an important role in the pathogenesis of atopic dermatitis. To examine whether CCR4 single nucleotide polymorphism (SNP) is associated with susceptibility to atopic dermatitis, we investigated the allele and genotype frequencies of C1014T SNP of CCR4 in 198 Japanese patients with atopic dermatitis and controls by a PCR-restriction fragment length polymorphism method. There was no significant difference in allele or genotype frequencies between patients with atopic dermatitis and controls.

Concerted expression of eotaxin-1, eotaxin-2, and eotaxin-3 in human bronchial epithelial cells.

Eotaxin-1/CCL11, eotaxin-2/CCL24, and eotaxin-3/CCL26 bind specifically and exclusively to CC chemokine receptor (CCR) 3, which is a potential therapeutic target in treating the peribronchial eosinophilia associated with allergic airway diseases. Bronchial epithelial cells represent an important source of chemokines, and thus we investigated in vitro and in vivo expression of eotaxin-2 and eotaxin-3 in bronchial epithelial cells in comparison with that of eotaxin-1. Immunohistochemistry showed increased expression of both eotaxin-2 and eotaxin-3 in addition to eotaxin-1 in asthmatics.

Expression and function of Toll-like receptors in eosinophils: activation by Toll-like receptor 7 ligand.

We investigated the expression of a panel of Toll-like receptors (TLRs) and their functions in human eosinophils. Eosinophils constitutively expressed TLR1, TLR4, TLR7, TLR9, and TLR10 mRNAs (TLR4 greater than TLR1, TLR7, TLR9, and TLR10 greater than TLR6). In contrast, neutrophils expressed a larger variety of TLR mRNAs (TLR1, TLR2, TLR4, TLR6, TLR8 greater than TLR5, TLR9, and TLR10 greater than TLR7).

Effects of suplatast tosilate on allergic eosinophilic airway inflammation in patients with mild asthma.

Background: Bronchial asthma is a chronic inflammatory disease characterized mainly by infiltration of the airway mucosa by various inflammatory cells, notably eosinophils. T(H)2-type cytokines are suggested to be deeply involved in the pathogenesis of asthma.

Objective: We sought to determine the suppressive effects of suplatast tosilate, an inhibitor of T(H)2-type cytokines, on eosinophilic inflammation of the bronchial mucosa in patients with mild asthma.

Induction of basophil desensitization in physiological medium: enhancement after IgE-dependent upregulation of surface IgE binding on basophils.

Background: Although the ability of basophils to release mediators, called releasability, may be an important aspect which influences the proinflammatory role of these cells, clinical approaches aiming at the depletion of the releasability have not been established. We examined whether the desensitization procedure in Ca(2+)-containing physiological conditions can make basophils completely unresponsive to IgE-mediated stimulation, and whether basophil desensitization is affected by the surface IgE levels.

Methods: Human peripheral blood basophils were cultured with low concentrations of anti-IgE antibody or recombinant mite allergen.

Attenuation of airway hyperresponsiveness in a murine asthma model by neutralization of granulocyte-macrophage colony-stimulating factor (GM-CSF).

Asthma is recognized as an inflammatory disease in which various cytokines are involved. Among these, granulocyte-macrophage colony-stimulating factor (GM-CSF) is known to play a critical role in the survival of eosinophils and in the activation of antigen-presenting cells (APC). We studied the effects of neutralization of GM-CSF in a murine model of asthma, to elucidate its role in enhanced airway responsiveness and in airway inflammation.

Variations in the human Th2-specific chemokine TARC gene.

Th2-specific chemokine thymus and activation-regulated chemokine (TARC)/CC chemokine ligand (CCL)17 is highly implicated in the pathogenesis of Th-2-dominated allergic diseases such as bronchial asthma (BA) and atopic dermatitis (AD). We performed polymorphism screening of the coding and promoter regions of the TARC gene. We found two rare variations in the coding region of exon 3 (2134C>T and 2037G>A) and a single nucleotide polymorphism (SNP) in the 5'-flanking region (-431C>T).

[Usefulness of patient education and quality of life (QOL) evaluation in asthma patients].

Achieving successful treatment of bronchial asthma depends on its control by the patient. We implemented a program of educating asthma patients and conducted a QOL survey to objectively evaluate the patients'conditions. Thirty-nine asthma patients who were receiving treatment with an inhaled corticosteroid [beclomethasone dipropionate (BDP) ] on an outpatient basis at our hospital, received instructions on proper drug administration in cooperation with the Pharmacy department of our hospital.

Mutation screening of the muscarinic m2 and m3 receptor genes in asthmatics, outgrow subjects, and normal controls.

Muscarinic receptors are important in the development of airway hyperresponsiveness. In some patients with asthma and in animal models of hyperreactivity, functional abnormalities in these receptors are suggested to contribute to disease. Here, we have screened for single nucleotide polymorphisms in the coding region of human muscarinic m2 and m3 receptor genes using direct fluorescence sequencing.

[A case report of lymphomatoid granulomatosis (LYG) with spontaneous attenuation].

70 years old woman was admitted to our hospital for the evaluation of multiple nodular shadows on chest X-ray. She had no clinical symptoms despite of mild increase of LDH and decrease of PaO2 on laboratory examination. Video associated thoracic surgery was performed to obtain lung tissue for the pathological diagnosis.

Destructive pulmonary embolism in a patient with community-acquired staphylococcal bacteremia.

We report a 17-year-old man with destructive pulmonary embolism caused by Staphylococcus aureus bacteremia. The patient was not immunocompromised and had neither underlying diseases nor risk factors, such as concomitant influenza viral infection, which exacerbate staphylococcal infections. The rapid and extensive progression of pulmonary involvement in all lung fields make this a rare case; there have been few reports in the literature describing a similar radiographic appearance in patients with community-acquired staphylococcal bacteremia.