Pathogenesis of Allergic Airway Inflammation

Center for Clinical and Translational Science, Creighton University School of Medicine, CRISS II, Room 510, Omaha, NE 68178, USA.
Current Allergy and Asthma Reports (Impact Factor: 2.77). 01/2010; 10(1):39-48. DOI: 10.1007/s11882-009-0081-7
Source: PubMed


Advances have been made in defining the mechanisms for the control of allergic airway inflammation in response to inhaled antigens. Several genes, including ADAM33, DPP10, PHF11, GPRA, TIM-1, PDE4D, OPN3, and ORMDL3, have been implicated in the pathogenesis and susceptibility to atopy and asthma. Growing evidence associates asthma with a systemic propensity for allergic T-helper type 2 cytokines. Disordered coagulation and fibrinolysis also exacerbate asthma symptoms. Balance among functionally distinct dendritic cell subsets contributes to the outcome of T-cell-mediated immunity. Allergen-specific T-regulatory cells play a pivotal role in the development of tolerance to allergens and immune suppression. The major emphasis on immunotherapy for asthma during the past decade has been to direct the immune response to a type 1 response, or immune tolerance. In this review, we discuss the current information on the pathogenesis of allergic airway inflammation and potential immunotherapy, which could be beneficial in the treatment of airway inflammation, allergy, and asthma.

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    • "Asthma is a chronic disease associated with airway hyperresponsiveness, airway obstruction, and airway remodelling [1, 2]. The principal pathophysiology of asthma is chronic inflammation of the lower respiratory tract [3]. "
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    ABSTRACT: The purpose of this study was to compare the effect and toxicity of organic selenium (Pro-Se) with inorganic selenium (IOSe) in preventing asthma in ovalbumin-induced asthmatic mice. After the mice were treated orally with Pro-Se and IOSe, respectively, the plasma Se levels, Se accumulation in liver and kidney, tumor necrosis factor alpha (TNF- α ), interleukin 1 beta (IL-1 β ), oxidative stress, and NF- κ B activation in lung were examined. The results showed that the serumal Se levels in the mice fed the Pro-Se were significant (P < 0.01) elevations. It results in restoration of the level of endogenous antioxidant enzyme, lower levels of TNF- α and IL-1 β , and activated NF- κ B in the asthmatic mice. Our experiments have demonstrated profound differences between the activities of organic selenium and inorganic selenium in experimental conditions. These data provide an important proof of the concept that organic selenium might be a new potential therapy for the management of childhood asthma in humans.
    Evidence-based Complementary and Alternative Medicine 02/2014; 2014:182817. DOI:10.1155/2014/182817 · 1.88 Impact Factor
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    • "Asthma is a chronic inflammatory disease of the airways characterized by infiltration of immune cells, hypersensitivity, bronchoconstriction, airway obstruction, and airway remodeling (1). One of the most common types of asthma is allergic asthma. "
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    ABSTRACT: Hematopoietic stem and progenitor cells contribute to allergic inflammation. Pro-inflammatory cytokines that are generated following allergen challenge can impact the differentiation of hematopoietic progenitor cells leading to increased production of effector cells such as eosinophils and basophils, which are key cells involved in the pathogenesis of allergic airway inflammation. Homing of stem cells to the lungs is associated with inflammatory and remodeling changes in asthmatics. Factors that modulate the differentiation and increased migration of stem cells to the site of inflammation in asthma remain to be defined. Stem cells can mature at the site of inflammation in response to inflammatory mediators and other components in the milieu. While the available data suggest that hematopoietic cells traffic to target tissues, the molecular factors underlying in situ differentiation have yet to be specified. Here, we critically evaluate the potential role of hematopoietic progenitors in contributing to the increased immune cell infiltrate in allergic asthma and the factors that drive their differentiation.
    Frontiers in Immunology 12/2013; 4:428. DOI:10.3389/fimmu.2013.00428
    • "Under conditions of chronic inflammation in allergic asthma, neutrophils along with eosinophils are the first cells to be recruited to inflammatory sites (Baggiolini, 1998; Agrawal and Shao, 2010). Neutrophils, which are the most abundant leukocytes in the blood, use two basic strategies to eliminate microorganisms (Guimaraes- Costa et al., 2012). "
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    ABSTRACT: Asthma is frequently caused and/or exacerbated by sensitization to fungal allergens, which are ubiquitous in many indoor and outdoor environments. Severe asthma with fungal sensitization is characterized by airway hyperresponsiveness and bronchial constriction in response to an inhaled allergen that is worsened by environmental exposure to airborne fungi and which leads to a disease course that is often very difficult to treat with standard asthma therapies. As a result of complex interactions among inflammatory cells, structural cells, and the intercellular matrix of the allergic lung, patients with sensitization to fungal allergens may experience a greater degree of airway wall remodeling and progressive, accumulated pulmonary dysfunction as part of the disease sequela. From their development in the bone marrow to their recruitment to the lung via chemokine and cytokine networks, eosinophils form an important component of the inflammatory milieu that is associated with this syndrome. Eosinophils are recognized as complex multi-factorial leukocytes with diverse functions in the context of allergic fungal asthma. In this review, we will consider recent advances in our understanding of the molecular mechanisms that are associated with eosinophil development and migration to the allergic lung in response to fungal inhalation, along with the eosinophil's function in the immune response to and the immunopathology attributed to fungus-associated allergic pulmonary disease.
    Frontiers in Pharmacology 02/2013; 4:8. DOI:10.3389/fphar.2013.00008 · 3.80 Impact Factor
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