Inflammation in allergic asthma: Initiating events, immunological response and risk factors (original) (raw)
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IgE regulation and roles in asthma pathogenesis
Journal of Allergy and Clinical Immunology, 2001
Asthma and the predisposition to produce IgE are inherited as linked traits in families. In patients IgE levels correlate with asthma severity and bronchial hyperresponsiveness. The concept that IgE plays a critical role in asthma pathogenesis has driven the development of IgE blockers, which are currently being introduced into clinical use. This review focuses on the mechanisms whereby IgE participates both in immediate hypersensitivity responses in the airways and in the induction of chronic allergic bronchial inflammation. The molecular genetic events that give rise to IgE production by B cells and the cellular and cytokine factors that support IgE production in the bronchial mucosal microenvironment are discussed. It is clear that much remains to be learned regarding the roles of IgE in asthma and the genetic and environmental influences that lead to its production. Over the next few years, the emerging experience with anti-IgE in patients will provide a more complete understanding of the mechanisms whereby IgE contributes to disease, as well as the therapeutic potential of its inhibition. (J Allergy Clin Immunol 2001;107:429-40.)
dIvergEnt: How IgE Axis Contributes to the Continuum of Allergic Asthma and Anti-IgE Therapies
International journal of molecular sciences, 2017
Asthma is an airway disease characterised by chronic inflammation with intermittent or permanent symptoms including wheezing, shortness of breath, chest tightness, and cough, which vary in terms of their occurrence, frequency, and intensity. The most common associated feature in the airways of patients with asthma is airway inflammation. In recent decades, efforts have been made to characterise the heterogeneous clinical nature of asthma. The interest in improving the definitions of asthma phenotypes and endotypes is growing, although these classifications do not always correlate with prognosis nor are always appropriate therapeutic approaches. Attempts have been made to identify the most relevant molecular and cellular biomarkers underlying the immunopathophysiological mechanisms of the disease. For almost 50 years, immunoglobulin E (IgE) has been identified as a central factor in allergic asthma, due to its allergen-specific nature. Many of the mechanisms of the inflammatory casca...
The Immunology of Asthma and Allergic Rhinitis
Rhinosinusitis, 2019
The immune system is a complex collection of cells, tissues, and chemical mediators positioned throughout the body, whose primary purpose is to protect us against infection. However, its function is not only fundamental in protection from infectious disease but also provides aberrant response in allergens such as with asthma and allergic rhinitis. Allergic diseases like asthma and allergic rhinitis are characterized by a distinct type of inflammatory response, driven by immunoglobulin E (IgE)-dependent mechanisms. In asthma and allergic rhinitis, the inflammatory response is mediated by interaction of several immune cells (monocytes, lymphocytes, and polymorphonuclear cells) and cellular chemical mediators. In particular, atopic allergic response leads to destruction of multiple target cells such as epithelial, parenchymal and vascular and connective tissue of the airways. In addition, in inflammatory response in asthma and allergic rhinitis, sensory nerves are sensitized, leading to clinical manifestations. Sneezing and coughing are hypersensitivity responses of sensory nerves in allergic rhinitis and asthma, respectively. Similarly, nasal congestion and discharge in allergic rhinitis are due to vasodilatation that leads to plasma exudates as well as mucous secretion. The allergic inflammatory response is regulated by several transcription factors, particularly nuclear factor-κb (NF-κB), GATA-3 protein 3, and GATA binding protein.
New aspects on inflammation in allergic diseases
Allergologia et Immunopathologia, 2006
Background: Allergic disease has currently reached epidemic proportions, with a high percentage of individuals in the developed world exhibiting an allergic response after exposure to some common environmental factors. Although new strategies for the treatment and management of allergic diseases have decreased the mortality rate, a high percentage of affected persons still require frequent hospitalization and experience decreased quality of life. Methods: An internet-based literature search was performed for recent contributions on the underlying mechanisms provoking an allergic response and their potential for therapeutic approaches. Results: Novel concepts on allergic responses have emerged: allergic disease may result from an imbalance between allergen activation of regulatory T cells and effector T helper 2 cells (Th2), a process in which dendritic cells are key players. Cytokines such as interleukin (IL)-6, IL-21, IL-25, and human thymic stromal lymphopoietin (TSLP) seem to be important contributors in allergic processes. New data on IgE effector responses and on the IgE-independent mechanisms involved in allergic reactions have resolved some unanswered questions about these reactions. Conclusions: These new findings on allergic diseases have important implications for diagnosis and management, with potential improvements in prevention and treatment, which could provide a cure in the future.
2020
The immune system is a complex collection of cells, tissues, and soluble mediators positioned throughout the body, whose primary purpose is to protect us against infection however its function is fundamental not only in protection from infectious disease but also as a consequence of an aberrant response in allergy. Asthma is much more than a T cell-mediated disease, and innate epithelial and immune cell functions are critical in its pathogenesis. A hyperactive type 2 immune response contributes to the pathogenesis of asthma in a subgroup of patients however not in all patients with asthma. Blood, and airway biomarkers of increased, IL4, IL5, IL-13 activity(eosinophilia) can identify those with a socalled “Th2-high” type of disease. The pathophysiology of T2 low asthma is not well under-stood, but is characterized by the absence of T2 markers of activation and downstream signatures, such as eosinophilia. The interaction between the airway epithelium and the inhaled environment is cru...
Anti-IgE efficacy in murine asthma models is dependent on the method of allergen sensitization
Journal of Allergy and Clinical Immunology, 2001
Background: Murine models used to delineate mechanisms and key mediators of asthma have yielded conflicting results and suggest that the dominant mechanism and mediators required for disease induction differ depending on the model and method of allergen sensitization used. Objective: The goal of this study was to determine whether the mode of allergen sensitization influenced the role that IgE had in allergen-induced pulmonary eosinophilic inflammation. Methods: Mice were exposed to dust mite extract in 2 models of allergic inflammation that differed in the method of sensitization. We compared sensitization by aerosol exposure with and without concomitant human respiratory syncytial virus infection with sensitization by means of systemic (intraperitoneal) exposure with adjuvant. After sensitization, animals were similarly challenged with aerosolized allergen. Animals were treated with anti-IgE mAb to deplete IgE and to determine its role in the induction of allergic inflammation and mucosa pathology in these models.
Immunity and asthma: friend or foe?
Oriental Pharmacy and Experimental Medicine, 2008
Immunity is responsible for the defense mechanism of the body but in case of autoimmune diseases, its role gets diverted. Like so many other diseases, asthma is also considered as one of the most common autoimmune diseases to be occurring in community. Asthma is defined as a chronic inflammatory airway disease that is characterized by airway hyper reactivity and mucus hypersecretion that result in intermittent airway obstruction. The incidence of allergic asthma has almost doubled in the past two decades. Although, precise causative mechanism of asthma is unknown, but several mechanisms have been proposed that is immunological, pharmacological and genetic mechanisms, and airway and neurogenic inflammation. The inflammatory process observed in the asthmatic patients is the final result of a complex network of interactions between various immunological cell lineages, its mediators and secreted substances. Thus, among the mechanisms proposed, the immunological one plays a key role. Through this article, we have tried to provide some insight into immunological mechanisms in pathogenesis of asthma.