Challenges and Outcomes of the First Stem Cell Transplant Program in Tanzania, East Africa.

Introduction: Due to the significant resources involved in creating HSCT programs there is a significant disparity in the availability of this treatment modality between the developed and developing countries. This manuscript details the process and the outcomes of the first HSCT program in East Africa which was started at Muhimbili National Hospital (MNH) in Dar-es-Salaam, Tanzania.

Materials And Methods: Information and data were collected on the processes which had been implemented for starting the HSCT program at MNH.

An asthma patient with steroid-resistant decrease in peak expiratory flow after the Great East Japan earthquake showing spontaneous recovery after 1 month.

People living in Japan were affected in various ways after the Great East Japan earthquake of March 11, 2011. A 52-year-old female asthma patient not directly affected by the disaster experienced a decrease in peak expiratory flow (PEF) immediately after the earthquake. Despite increasing the inhaled and oral corticosteroid doses, her PEF did not recover.

Eosinophils are required for the induction of bronchial hyperresponsiveness in a Th transfer model of BALB/c background.

Background: Helper T (Th) cells are deeply involved in the pathophysiology of bronchial asthma, such as eosinophilic inflammation, bronchial hyperresponsiveness (BHR), airflow limitation and remodeling. It is still unclear whether Th cells contribute to BHR independently of eosinophilic inflammation. The double GATA (dblGATA) site is a high-affinity GATA-binding site in the GATA-1 promoter.

[Knowledge of guideline for asthma and a demand at the pharmacy--questionnaire based exploration].

Background: To achieve a good control for asthma, cooperation of pharmacists is necessary. It is important to establish the system that the patients easily obtain advice about asthma from pharmacists and to spread the guideline.

Methods: For the first step, we explore the knowledge and usage of asthmatic guideline among pharmacists in the drug stores in this study.

Evaluation of cysteinyl leukotriene-induced contraction of human cultured bronchial smooth muscle cells.

Background: Cysteinyl leukotrienes (cysLTs) are major mediators involved in bronchial asthma, particularly bronchial constriction. However, a contractile response of human bronchial smooth muscle cells (hBSMCs) to cysLTs has not been well characterized at cellular level.

Methods: A contraction assay using collagen gel embedded with cultured hBSMCs was established to analyze contractile responses at cellular level.

Murine Th clones confer late asthmatic response upon antigen challenge.

Background: Helper T (Th) cells are deeply involved in the pathophysiology of bronchial asthma, such as eosinophilic inflammation, bronchial hyperresponsiveness and remodeling. However, it is still unclear how Th cells contribute to airflow limitation, another cardinal feature of bronchial asthma.

Method: Unprimed BALB/c mice were transferred with ovalbumin (OVA)-reactive Th clones.

Effect of formoterol on allergen-induced cytokine synthesis by atopic asthmatics.

Background: Effect of formoterol, long-acting beta(2 )agonists, on T cell cytokine synthesis was examined.

Methods: Human peripheral blood mononuclear cells were obtained from atopic asthmatics, and stimulated with Dermatophagoidesfarinae extract. Various concentrations of formoterol were added from the start of some cultures.

IL-9 production by peripheral blood mononuclear cells of atopic asthmatics.

Background: IL-9 might play a critical role in pathogenesis and development of atopic asthma, but there are few reports on allergen-specific IL-9 production by peripheral blood mononuclear cells (PBMCs) obtained from adult asthmatics.

Methods: PBMCs were obtained from adult atopic asthmatics and incubated with Dermatophagoides farinae(Der f) extract for the designated time periods. The resulting supernatants were assayed for IL-9 by specific sandwich ELISA.

Genetic factors in the treatment of bronchial asthma.

Owing to the recent vast progress in analytical tools and procedures to elucidate the relationship between genes and diseases, many candidate genes leading to the development of bronchial asthma have been reported. However, the quantitative phenotypes of asthma, such as decrease in forced expiratory volume in the first second, serum hyper-IgE, bronchial hyperresponsiveness and blood hyper-eosinophilia, do not represent this disease completely. On the other hand, eosinophilic inflammation of the bronchial mucosa represents accurately the feature of bronchial asthma, although accurate quantification of its status is difficult.

Th2-cell-mediated chemokine synthesis is involved in allergic airway inflammation in mice.

Eosinophilic inflammation in the bronchial mucosa has been recognized as a prominent pathological feature of bronchial asthma. Th2 cells have been implicated in the local infiltration and activation of eosinophils. The migration of eosinophils as well as Th2 cells is controlled by chemokines, suggesting a crucial role of chemokines in the pathogenesis of bronchial asthma.

IL-2-induced IL-13 production by allergen-specific human helper T cell clones.

Background: Interleukin (IL)-5 and IL-13 are important cytokines in allergic diseases such as asthma and atopic dermatitis. We have reported that the production of IL-5 and IL-13 by mite-responsive T helper cells (Th) is controlled under similar signal requirements, but precise mechanisms are not yet well characterized.

Methods: Allergen-specific Th clones were established from peripheral blood lymphocytes of atopic asthmatics, and cytokine synthesis in response to various stimuli was determined by specific ELISAs.

[Clinical courses of 18 cases with food-dependent exercise-induced anaphylaxis].

Eighteen cases (7 males and 11 females) of food-dependent exercise-induced anaphylaxis were observed for several years. The age of the patients at the first visit to our hospital ranged from 9 to 43 years (average 24.3 years).

Primary role of CD4+ T cells and supplemental role of mast cells in allergic pulmonary eosinophilia.

Background: We have recently demonstrated that allergic eosinophilic inflammation is transferred to unprimed mice by infusing IL-5-producing CD4+ T cells. The contribution of mast cells to the development of eosinophilic inflammation is controversial.

Methods: To clarify the possible different roles of CD4+ T cells and mast cells in eosinophilic inflammation, we compared antigen-induced airway eosinophilia between mast-cell-deficient mice (WBB6F1-W/W(v)) and their congenic normal littermates (WBB6F1-+/+).

Comparison of sensitization to crude and purified house dust mite allergens in inbred mice.

To establish a murine model for house dust mite allergy to purified mite allergens, we studied the immune response to two major mite allergens, native Dermatophagoides farinae 1 (nDer f 1) and recombinant Der f 2 (rDer f 2), and crude mite extract in four mouse strains, A/J, BALB/c, C57BL/6, and C3H/He. Mice were immunized with mite extract, nDer f 1 or rDer f 2, three times at 2-week intervals. Then mice were examined to determine status of sensitization to the antigen.

IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice.

We have recently demonstrated that airway eosinophilic inflammation can be transferred to unprimed mice by infusion of IL-5-producing T cell clones. In this study, we investigated the effects of dexamethasone and cyclosporin A on the airway eosinophilic inflammation in mice transferred with T cell clones. An ovalbumin-reactive T cell clone, KW29, produced IL-5 as well as IL-2 and IL-4 upon stimulation with relevant antigen.

Evidence that cyclosporin A and dexamethasone inhibit allergic airway eosinophilic inflammation via suppression of interleukin-5 synthesis by T cells.

1. We have recently demonstrated that airway eosinophilic inflammation can be transferred to unprimed mice by infusing interleukin (IL)-5-producing T cell clones. Using that murine model, we performed this study to delineate the mechanism of cyclosporin A and dexamethasone to inhibit allergic airway eosinophilic inflammation.

Hyposensitization to allergic reaction in rDer f 2-sensitized mice by the intranasal administration of a mutant of rDer f 2, C8/119S.

C8/119S is a mutant of recombinant Der f 2 (rDer f 2), and lacks a disulphide bond possessed by wild-type rDer f 2. In humans and mice, C8/119S has a very weak IgE-binding capacity compared with the wild-type, but possesses a T cell reactivity comparable to that of the wild-type. C8/119S may thus be a safe immunotherapeutic agent for house dust mite allergy.

Effects of oral hyposensitization with recombinant Der f2 on immediate airway constriction in a murine allergic model.

Recombinant Der f2 (rDer f2) has recently been developed as a promising allergen for the diagnosis and immunotherapy of house-dust mite allergy, and studies in immunology. The aim of the present study was to evaluate whether oral administration of rDer f2 could suppress an immediate allergic reaction in mice sensitized with mite allergen. We developed a murine allergic model that showed bronchoconstriction after inhalation of rDer f2, and studied the effect of oral administration of rDer f2 on the reaction.

A selective type 4 phosphodiesterase inhibitor, T-440, modulates intracellular cyclic AMP level and interleukin-2 production of Jurkat cells.

Effect of a selective type 4 phosphodiesterase (PDE4) inhibitor, T-440, on intracellular cyclic AMP (cAMP) level and interleukin (IL)-2 production of Jurkat cells was investigated. T-440 suppressed both cAMP-PDE activities in cytosolic and membrane fractions of Jurkat cells. Intracellular cAMP level in Jurkat cells was elevated by PGE2 and forskolin but not by T-440.

Cellular and molecular mechanisms of IL-5 synthesis in atopic diseases: a study with allergen-specific human helper T cells.

Background: Cytokines produced by helper T cells are intimately involved in chronic allergic diseases associated with eosinophilic inflammation.

Objective: We investigated the production of IL-5, a potent growth factor and chemotactic factor for eosinophils, by CD4+ T lymphocytes in patients with asthma.

Methods: Allergen-specific T cell clones and T cell hybridomas were established from the peripheral blood lymphocytes of patients with asthma, and the responses to various stimuli were determined.

Development of lung eosinophilic inflammation by the infusion of IL-5-producing T cell clones.

To delineate the critical role of T cells on asthma, we tested whether eosinophilic inflammation of the bronchial mucosa is induced by transfer of IL-5-producing T cell clones, in the absence of antigen-specific immunoglobulins (IgE, A and G). Ovalbumin-specific T cell clone, FI5, that produced IL-5 upon challenge with relevant antigen was established. Eosinophilic inflammation of the lung occurred when unprimed mice were transferred with FI5 and challenged by the inhaled antigen.

Inhibition of airway inflammation in rDer f 2-sensitized mice by oral administration of recombinant der f 2.

Recombinant Der f 2 (rDer f 2) is a promising new allergen expected to improve the diagnosis and immunotherapy of house dust mite allergy and to further immunological studies. To evaluate the hyposensitizing activity of rDer f 2 to mite allergy, we examined the effect of its oral administration on allergic inflammation in A/J mice immunized with mite allergens. A/J mice immunized with rDer f 2 alone or rDer f 2 + crude mite extract were orally given 0 (control), 0.