Allergic Asthma Immunopathogenesis: Immunopathology of the Allergic Asthma
Allergic Asthma Immunopathogenesis: Immunopathology of the Allergic Asthma
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The book "Immunopathology of the Allergic Asthma" provides a new understanding of the immunopathogenesis and allergo-inflammation mechanisms of asthma,and cell signaling pathways that can be used for research purposes. It is important to understand the molecular pathways and pathophysiology of asthma in order to better understand the disease and develop effective treatments.
Format: Paperback / softback
Length: 208 pages
Publication date: 31 May 2024
Publisher: Elsevier Science Publishing Co Inc
Immunopathology of the Allergic Asthma presents a novel perspective on the pathophysiology of allergic asthma by delving into the immunopathogenesis and allergo-inflammation mechanisms of the disease, as well as cell signaling pathways that hold immense potential for various research purposes, including the design of anti-asthma treatments and target therapies for scientists and researchers. Given the chronic and complex nature of asthma, a condition that has witnessed a global increase in mortality and morbidity rates, conventional treatments for asthma often fail to effectively control the disease or prevent simple inflammation and alleviate shortness of breath. Consequently, a deeper understanding of its molecular pathways and pathophysiology is essential to enhance our comprehension of this ailment.
The immune system plays a crucial role in the development and progression of allergic asthma. It is characterized by the presence of IgE antibodies, which are specific to allergens and trigger the release of inflammatory chemicals such as histamine and leukotrienes. These chemicals cause the narrowing of the airways, leading to symptoms such as wheezing, coughing, and shortness of breath.
The immunopathogenesis of allergic asthma involves several stages. Firstly, exposure to allergens leads to the activation of immune cells, such as mast cells and basophils, which release inflammatory mediators. These mediators then interact with other immune cells, such as T cells and B cells, to amplify the immune response. Additionally, the presence of certain genetic predispositions can increase the risk of developing allergic asthma.
Allergo-inflammation is another key mechanism in the pathophysiology of allergic asthma. It involves the activation of immune cells and the release of inflammatory mediators, which contribute to the narrowing of the airways and the development of symptoms. The inflammation in allergic asthma is characterized by the presence of eosinophils, which are white blood cells that produce inflammatory chemicals.
Cell signaling pathways are also important in the pathophysiology of allergic asthma. These pathways involve the communication between cells and the regulation of various cellular processes. For example, the JAK-STAT pathway is involved in the regulation of immune cell function and the production of inflammatory mediators. Other signaling pathways, such as the PI3K-AKT pathway, are involved in the regulation of cell growth and survival.
Understanding the immunopathogenesis and allergo-inflammation mechanisms of allergic asthma is crucial for developing effective treatments and therapies. Researchers are exploring various approaches, such as immunotherapy and targeted therapy, to treat allergic asthma. Immunotherapy involves the administration of allergens to desensitize the immune system, while targeted therapy targets specific cells and signaling pathways involved in the disease.
In conclusion, the immunopathogenesis and allergo-inflammation mechanisms of allergic asthma are complex and multifaceted. By understanding these mechanisms, researchers can develop new treatments and therapies that improve the quality of life for individuals with allergic asthma. Further research is needed to fully comprehend the molecular pathways and pathophysiology of allergic asthma and to identify new targets for treatment.
Weight: 346g
Dimension: 227 x 171 x 15 (mm)
ISBN-13: 9780443155024
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