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Related Concept Videos

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

Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids

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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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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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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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Antiasthma Drugs: Muscarinic Receptor Antagonists01:20

Antiasthma Drugs: Muscarinic Receptor Antagonists

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Muscarinic receptor antagonists, also known as antimuscarinic agents, are a class of bronchodilators used to treat asthma, although they are more commonly used to treat COPD. They work by inhibiting the action of acetylcholine (ACh), a neurotransmitter, on muscarinic receptors found in the airways.
Antimuscarinic agents compete with ACh for the same binding site on the muscarinic receptors. By binding to these receptors, they inhibit the downstream effects of ACh and block the parasympathetic...
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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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Related Experiment Video

Updated: Sep 14, 2025

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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Oncostatin M Drives Th2 Polarized Allergic Airway Inflammation Through Fibroblast Reprogramming and Endoplasmic

Huanping Zhang1, Xiaoxue Chen1, Le Liu2

  • 1Department of Allergy Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, People's Republic of China.

International Journal of Nanomedicine
|July 21, 2025
PubMed
Summary

Oncostatin M (OSM) drives allergic airway inflammation by reprogramming fibroblasts via endoplasmic reticulum stress. Targeting the OSM-ERS-IL-4 pathway with ATF4 siRNA significantly reduces asthma symptoms.

Keywords:
ERSIL-4OSMOncostatin Mairway fibroblastsallergic airway inflammationendoplasmic reticulum stress

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Area of Science:

  • Immunology
  • Cell Biology
  • Respiratory Medicine

Background:

  • Allergic airway inflammation, a key feature of asthma, involves Th2 cytokines and eosinophils.
  • Airway epithelium releases cytokines like Oncostatin M (OSM), influencing allergic responses.

Purpose of the Study:

  • Investigate OSM's role in dust mite extract (DME)-induced allergic airway inflammation.
  • Identify the mechanism by which OSM promotes Th2-polarized inflammation.

Main Methods:

  • Established a murine model of DME-induced airway inflammation.
  • Treated mice with CelEd, a nanoparticle delivering ATF4 siRNA to fibroblasts.

Main Results:

  • DME exposure increased OSM expression in airway epithelial cells and human cell lines.
  • OSM administration mimicked allergic inflammation in mice.
  • OSM induced IL-4 production via fibroblast endoplasmic reticulum stress (ERS) and the PERK-eIF2α-ATF4 pathway.
  • Fibroblast-specific ATF4 knockdown ameliorated allergic pathology.

Conclusions:

  • OSM is critical in allergic airway inflammation.
  • The OSM-ERS-IL-4 axis represents a potential therapeutic target for asthma and allergic diseases.