Allergic Asthma

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Jae Hyun Lee - One of the best experts on this subject based on the ideXlab platform.

  • soluble cd93 in Allergic Asthma
    Scientific Reports, 2020
    Co-Authors: Hye Jung Park, Heejae Han, Kyung Hee Park, Kyoung Yong Jeong, Jung Won Park, Jae Hyun Lee
    Abstract:

    CD93 has been shown critical roles in inflammatory and immune diseases. However, in Allergic Asthma, the potential roles of soluble CD93 (sCD93) have not been well studied. We conducted house dust mite (HDM) stimulation with Der p 1 in BEAS-2B and U937 cells, followed by treatment with dexamethasone or small interfering RNA against CD93. A HDM-induced murine Allergic Asthma model was also established. We estimated the power of sCD93 to predict Allergic Asthma in a retrospective post-hoc analysis containing 96 human samples. HDM-stimulated BEAS-2B cells showed increased mRNA expression levels of IL-6, IL-8, IL-33, TSLP, and CD93. The CD93 level in culture supernatants steadily increased for 24 h after allergen stimulation, which was significantly suppressed by both dexamethasone and CD93 silencing. CD93 silencing increased IL-6 and TSLP, but not IL-33 levels in culture supernatants. HDM-induced Asthma mice showed significant airway hyperresponsiveness and inflammation with Th2 cytokine activation, along with decreased CD93 expression in bronchial epithelial cells and lung homogenates but increased serum CD93 levels. The sCD93 level in Asthma patients was significantly higher than that in healthy controls and could predict Asthma diagnosis with moderate sensitivity (71.4%) and specificity (82.4%) (AUC = 0.787, P < 0.001). The level of sCD93 which has potential role to predict Asthma significantly increased after HDM stimulation via IL-6 and TSLP in vitro and in vivo.

  • Soluble CD93 in Allergic Asthma
    Scientific reports, 2020
    Co-Authors: Hye Jung Park, Heejae Han, Kyung Hee Park, Kyoung Yong Jeong, Jung Won Park, Jae Hyun Lee
    Abstract:

    CD93 has been shown critical roles in inflammatory and immune diseases. However, in Allergic Asthma, the potential roles of soluble CD93 (sCD93) have not been well studied. We conducted house dust mite (HDM) stimulation with Der p 1 in BEAS-2B and U937 cells, followed by treatment with dexamethasone or small interfering RNA against CD93. A HDM-induced murine Allergic Asthma model was also established. We estimated the power of sCD93 to predict Allergic Asthma in a retrospective post-hoc analysis containing 96 human samples. HDM-stimulated BEAS-2B cells showed increased mRNA expression levels of IL-6, IL-8, IL-33, TSLP, and CD93. The CD93 level in culture supernatants steadily increased for 24 h after allergen stimulation, which was significantly suppressed by both dexamethasone and CD93 silencing. CD93 silencing increased IL-6 and TSLP, but not IL-33 levels in culture supernatants. HDM-induced Asthma mice showed significant airway hyperresponsiveness and inflammation with Th2 cytokine activation, along with decreased CD93 expression in bronchial epithelial cells and lung homogenates but increased serum CD93 levels. The sCD93 level in Asthma patients was significantly higher than that in healthy controls and could predict Asthma diagnosis with moderate sensitivity (71.4%) and specificity (82.4%) (AUC = 0.787, P 

Dennis K. Ledford - One of the best experts on this subject based on the ideXlab platform.

  • Immunotherapy for Allergic Asthma
    Medical Clinics of North America, 2002
    Co-Authors: Nina C. Ramirez, Dennis K. Ledford
    Abstract:

    Specific allergen immunotherapy is an effective treatment of Allergic Asthma. Double-blind studies provide proof of benefit, although seasonal or intermittent Asthma consistently responds better than perennial Asthma. Advantages of immunotherapy compared with most pharmacotherapies include modification of the natural history of Allergic disease, reduction of need for chronic medication, and treatment of both upper and lower airway disease simultaneously. Improvements in immunotherapy occurred in the later portion of the twentieth century because of enhanced understanding of immunotherapy's mechanism of action, recognition of the dose effect, and improved quality and consistency of allergen vaccines. Purified inhibitors of specific mediators of the Allergic response, products of biotechnology, will probably lead to improvements of immunotherapy of Asthma in the twenty-first century. The future of immunotherapy and other immunomodulation of Allergic Asthma is promising.

Michelle M Epstein - One of the best experts on this subject based on the ideXlab platform.

  • Are mouse models of Allergic Asthma useful for testing novel therapeutics
    Experimental and Toxicologic Pathology, 2006
    Co-Authors: Michelle M Epstein
    Abstract:

    Experimental mouse Allergic Asthma is a reliable, clinically relevant facsimile of human disease. The focus here is to demonstrate that antigen-induced mouse Allergic Asthma is a useful model for testing novel therapeutics. Furthermore, it is especially crucial to treat mice during established disease, either during ongoing clinically manifest disease or to prevent disease relapses. In addition, our results indicate that lung Th2 resting memory cells are important targets for the treatment of Allergic Asthma.

  • Targeting memory Th2 cells for the treatment of Allergic Asthma.
    Pharmacology & therapeutics, 2005
    Co-Authors: Michelle M Epstein
    Abstract:

    Th2 memory cells play an important role in the pathogenesis of Allergic Asthma. Evidence from patients and experimental models indicates that memory Th2 cells reside in the lungs during disease remission and, upon allergen exposure, become activated effectors involved in disease exacerbation. The inhibition of memory Th2 cells or their effector functions in Allergic Asthma influence disease progression, suggesting their importance as therapeutic targets. They are allergen specific and can potentially be suppressed or eliminated using this specificity. They have distinct activation, differentiation, cell surface phenotype, migration capacity, and effector functions that can be targeted singularly or in combination. Furthermore, memory Th2 cells residing in the lungs can be treated locally. Capitalizing on these unique attributes is important for drug development for Allergic Asthma. The aim of this review is to present an overview of therapeutic strategies targeting Th2 memory cells in Allergic Asthma, emphasizing Th2 generation, differentiation, activation, migration, effector function, and survival.

  • Modeling Allergic Asthma: from in vitro assays to virtual patients
    Drug Discovery Today: Disease Models, 2004
    Co-Authors: Michelle M Epstein
    Abstract:

    Allergic Asthma is a complex disease of the respiratory tract characterized by allergen-induced breathlessness that is, orchestrated by the interaction of immune, inflammatory, and resident lung cells. Great strides have been made with in vitro and in vivo experimentation, but disease pathogenesis remains obscure. The combination of cellular, in vivo, and in silico modeling promises the eventual creation of a heterogeneous population of virtual patients to pursue unresolved issues in Allergic Asthma.

  • long lived th2 memory in experimental Allergic Asthma
    Journal of Immunology, 2002
    Co-Authors: Nazanin Mojtabavi, Gerhard Dekan, Georg Stingl, Michelle M Epstein
    Abstract:

    Although life-long immunity against pathogens is beneficial, immunological memory responses directed against allergens are potentially harmful. Because there is a paucity of information about Th2 memory cells in Allergic disease, we established a model of Allergic Asthma in BALB/c mice to explore the generation and maintenance of Th2 memory. We induced disease without the use of adjuvants, thus avoiding Ag depots, and found that unlike Allergic Asthma in mice immunized with adjuvant, immunizing with soluble and aerosol OVA resulted in pathological lung lesions resembling human disease. To test memory responses we allowed mice with acute disease to recover and then re-exposed them to aerosol OVA a second time. Over 400 days later these mice developed OVA-dependent eosinophilic lung inflammation, airway hyperresponsiveness, mucus hypersecretion, and IgE. Over 1 year after recuperating from acute disease, mice had persistent lymphocytic lung infiltrates, Ag-specific production of IL-4 and IL-5 from spleen and lung cells in vitro, and elevated IgG1. Moreover, when recuperated mice were briefly aerosol challenged, we detected early expression of Th2 cytokine RNA in lungs. Taken together, these data demonstrate the presence of long-lived Th2 memory cells in spleen and lungs involved in the generation of Allergic Asthma upon Ag re-exposure.

Hye Jung Park - One of the best experts on this subject based on the ideXlab platform.

  • soluble cd93 in Allergic Asthma
    Scientific Reports, 2020
    Co-Authors: Hye Jung Park, Heejae Han, Kyung Hee Park, Kyoung Yong Jeong, Jung Won Park, Jae Hyun Lee
    Abstract:

    CD93 has been shown critical roles in inflammatory and immune diseases. However, in Allergic Asthma, the potential roles of soluble CD93 (sCD93) have not been well studied. We conducted house dust mite (HDM) stimulation with Der p 1 in BEAS-2B and U937 cells, followed by treatment with dexamethasone or small interfering RNA against CD93. A HDM-induced murine Allergic Asthma model was also established. We estimated the power of sCD93 to predict Allergic Asthma in a retrospective post-hoc analysis containing 96 human samples. HDM-stimulated BEAS-2B cells showed increased mRNA expression levels of IL-6, IL-8, IL-33, TSLP, and CD93. The CD93 level in culture supernatants steadily increased for 24 h after allergen stimulation, which was significantly suppressed by both dexamethasone and CD93 silencing. CD93 silencing increased IL-6 and TSLP, but not IL-33 levels in culture supernatants. HDM-induced Asthma mice showed significant airway hyperresponsiveness and inflammation with Th2 cytokine activation, along with decreased CD93 expression in bronchial epithelial cells and lung homogenates but increased serum CD93 levels. The sCD93 level in Asthma patients was significantly higher than that in healthy controls and could predict Asthma diagnosis with moderate sensitivity (71.4%) and specificity (82.4%) (AUC = 0.787, P < 0.001). The level of sCD93 which has potential role to predict Asthma significantly increased after HDM stimulation via IL-6 and TSLP in vitro and in vivo.

  • Soluble CD93 in Allergic Asthma
    Scientific reports, 2020
    Co-Authors: Hye Jung Park, Heejae Han, Kyung Hee Park, Kyoung Yong Jeong, Jung Won Park, Jae Hyun Lee
    Abstract:

    CD93 has been shown critical roles in inflammatory and immune diseases. However, in Allergic Asthma, the potential roles of soluble CD93 (sCD93) have not been well studied. We conducted house dust mite (HDM) stimulation with Der p 1 in BEAS-2B and U937 cells, followed by treatment with dexamethasone or small interfering RNA against CD93. A HDM-induced murine Allergic Asthma model was also established. We estimated the power of sCD93 to predict Allergic Asthma in a retrospective post-hoc analysis containing 96 human samples. HDM-stimulated BEAS-2B cells showed increased mRNA expression levels of IL-6, IL-8, IL-33, TSLP, and CD93. The CD93 level in culture supernatants steadily increased for 24 h after allergen stimulation, which was significantly suppressed by both dexamethasone and CD93 silencing. CD93 silencing increased IL-6 and TSLP, but not IL-33 levels in culture supernatants. HDM-induced Asthma mice showed significant airway hyperresponsiveness and inflammation with Th2 cytokine activation, along with decreased CD93 expression in bronchial epithelial cells and lung homogenates but increased serum CD93 levels. The sCD93 level in Asthma patients was significantly higher than that in healthy controls and could predict Asthma diagnosis with moderate sensitivity (71.4%) and specificity (82.4%) (AUC = 0.787, P 

Nina C. Ramirez - One of the best experts on this subject based on the ideXlab platform.

  • Immunotherapy for Allergic Asthma
    Medical Clinics of North America, 2002
    Co-Authors: Nina C. Ramirez, Dennis K. Ledford
    Abstract:

    Specific allergen immunotherapy is an effective treatment of Allergic Asthma. Double-blind studies provide proof of benefit, although seasonal or intermittent Asthma consistently responds better than perennial Asthma. Advantages of immunotherapy compared with most pharmacotherapies include modification of the natural history of Allergic disease, reduction of need for chronic medication, and treatment of both upper and lower airway disease simultaneously. Improvements in immunotherapy occurred in the later portion of the twentieth century because of enhanced understanding of immunotherapy's mechanism of action, recognition of the dose effect, and improved quality and consistency of allergen vaccines. Purified inhibitors of specific mediators of the Allergic response, products of biotechnology, will probably lead to improvements of immunotherapy of Asthma in the twenty-first century. The future of immunotherapy and other immunomodulation of Allergic Asthma is promising.