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Related Concept Videos

Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

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Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
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Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

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Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
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Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

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Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
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Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids01:25

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Inhaled corticosteroids (ICS) are anti-inflammatory drugs used primarily in treating persistent asthma and providing long-term maintenance. They target the bronchial mucosa, the lining of the airways, to control inflammation, a critical factor in asthma progression and exacerbation.
ICS work through a multifaceted mechanism of action. They suppress the inflammatory response caused by the proliferation of TH cells. They also reduce the transcription of the IL-2 gene, which is involved in the...
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Antiasthma Drugs: Leukotriene Modifiers01:19

Antiasthma Drugs: Leukotriene Modifiers

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Leukotriene modifiers, or cysteinyl leukotriene receptor antagonists, are medications used to manage chronic asthma. These agents target specific inflammatory mediators produced during arachidonic acid metabolism, an essential process in generating inflammation in the body.
Leukotriene modifiers work through two distinct mechanisms:
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Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

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Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
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Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
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Cellular mechanisms underlying steroid-resistant asthma.

Ridhima Wadhwa1,2,3, Kamal Dua1,2,4,3, Ian M Adcock5

  • 1Centre for Inflammation, Centenary Institute, Sydney, Australia.

European Respiratory Review : an Official Journal of the European Respiratory Society
|October 23, 2019
PubMed
Summary
This summary is machine-generated.

Respiratory infections are linked to severe steroid-resistant asthma in adults. Novel models identified macrolides as potential therapies targeting mechanisms like microRNA-21.

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Area of Science:

  • Pulmonology
  • Immunology
  • Microbiology

Background:

  • Severe steroid-resistant asthma affects patients unresponsive to corticosteroids.
  • Disease heterogeneity and poorly understood mechanisms impede effective therapies.
  • Multiple endotypes and phenotypes, especially in adults, complicate understanding.

Purpose of the Study:

  • To investigate the association between respiratory infections and severe steroid-resistant asthma.
  • To identify novel therapeutic targets and mechanisms in this condition.
  • To develop and utilize experimental models for studying these associations.

Main Methods:

  • Development of novel experimental models to study respiratory infections in severe steroid-resistant asthma.
  • Analysis of immunological and inflammatory phenotypes.
  • Investigation of specific molecular pathways and inflammasomes.

Main Results:

  • Established a link between respiratory infections and severe steroid-resistant asthma in adults.
  • Identified macrolides as a potential therapeutic strategy.
  • Uncovered novel disease mechanisms including the microRNA-21/PI3K/HDAC2 axis and NLRP3 inflammasomes.

Conclusions:

  • Respiratory infections play a significant role in severe steroid-resistant asthma.
  • The identified molecular pathways and inflammasomes represent promising therapeutic targets.
  • Macrolides show potential for treating this challenging asthma subtype.