Related Experiment Video

Updated: Jan 4, 2026

Murine Model of Allergen Induced Asthma
08:05

Murine Model of Allergen Induced Asthma

Published on: May 14, 2012

41.1K

MIF signaling blocking alleviates airway inflammation and airway epithelial barrier disruption in a HDM-induced

Haibing Lan1, Liang Luo2, Yu Chen1

  • 1Department of Intensive Care Unit, The Second Affiliated Hospital of NanChang University, Nanchang 330006, People's Republic of China.

Cellular Immunology
|November 12, 2019
PubMed

Insights

Macrophage migration inhibitory factor (MIF) exacerbates house dust mite-induced asthma by promoting airway inflammation and barrier disruption. Blocking MIF ameliorates asthma symptoms and restores epithelial barrier function, highlighting MIF as a therapeutic target.

Area of Science:

  • Immunology
  • Respiratory Medicine
  • Cell Biology

Background:

  • Macrophage migration inhibitory factor (MIF) is implicated in asthma pathogenesis.
  • The specific role of MIF in house dust mite (HDM)-induced airway inflammation and epithelial barrier dysfunction remains unclear.

Purpose of the Study:

  • To investigate the contribution of MIF to HDM-induced Th2 cytokine production and E-cadherin dysfunction in asthma.
  • To explore the underlying mechanisms, including the role of aerobic glycolysis.

Main Methods:

  • Established a HDM-induced asthma mouse model and treated with MIF antagonist ISO-1.
  • Exposed 16HBE cells to HDM and recombinant human MIF (rhMIF), with interventions using MIF siRNA and PFKFB3 antagonist PFK15.
  • Assessed airway hyper-reactivity, inflammation, serum IgE, E-cadherin arrangement, cytokine release, and glycolytic flux.

Main Results:

  • MIF antagonism (ISO-1) in mice ameliorated airway hyper-reactivity, inflammation, elevated IgE, disrupted E-cadherin, and Th2 cytokine release.
  • HDM and rhMIF exposure in 16HBE cells caused barrier disruption, inflammation, and enhanced glycolysis, which were reversed by MIF siRNA.
  • PFK15 treatment reduced rhMIF-induced changes in 16HBE cells.

Conclusions:

  • MIF is a key mediator in HDM-induced airway inflammation and epithelial barrier disruption in asthma.
  • HDM induces asthma pathology via MIF-mediated enhancement of aerobic glycolysis, suggesting MIF as a potential therapeutic target.
Keywords:
Aerobic glycolysisAirway epithelial barrier disruptionAirway inflammationAsthmaMIF

More Related Videos

Assessment of Respiratory Function in Conscious Mice by Double-chamber Plethysmography08:58

Assessment of Respiratory Function in Conscious Mice by Double-chamber Plethysmography

Published on: July 10, 2018

43.9K
A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice09:58

A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice

Published on: April 13, 2010

23.2K

Related Concept Videos

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

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...
1.7K
Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

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.
1.1K
Antiasthma Drugs: Muscarinic Receptor Antagonists01:20

Antiasthma Drugs: Muscarinic Receptor Antagonists

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...
1.6K
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

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:
4.0K
Antiasthma Drugs: Methylxanthines01:24

Antiasthma Drugs: Methylxanthines

Theophylline, a member of the methylxanthine class of bronchodilators, has long been used in asthma management. While its exact mechanism of action is not fully understood, it is believed to have multiple effects on various cellular processes.
Theophylline is thought to inhibit phosphodiesterase enzymes, increasing intracellular levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). This rise in cAMP and cGMP concentrations stimulates cardiac function,...
1.5K
Antiasthma Drugs: Leukotriene Modifiers01:19

Antiasthma Drugs: Leukotriene Modifiers

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:
1.7K