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Related Concept Videos

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.
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:
Allergic Reactions02:06

Allergic Reactions

Overview
Asthma I: Introduction01:28

Asthma I: Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction and heightened bronchial responsiveness to a wide range of triggers. The underlying inflammation leads to airway swelling, mucus hypersecretion, and smooth muscle constriction, all of which narrow the airway lumen and impede airflow. Clinically, asthma presents with recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, symptoms that typically vary in intensity and...
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
Allergic Drug Reactions01:27

Allergic Drug Reactions

Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing numerous...

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Related Experiment Video

Updated: May 31, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

Pathophysiology of allergic inflammation.

Peter J Barnes1

  • 1National Heart and Lung Institute, Imperial College, London, UK. p.j.barnes@imperial.ac.uk

Immunological Reviews
|June 21, 2011
PubMed
Summary

Allergic inflammation involves complex cell interactions and mediators. Understanding these pathways, including epigenetic factors, is key to developing new therapies beyond corticosteroids.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pathophysiology

Background:

  • Allergic inflammation results from intricate interactions among various immune cells like mast cells, lymphocytes, and eosinophils.
  • These cells release numerous inflammatory mediators, including cytokines and chemokines, impacting target cells such as epithelial and vascular cells.
  • Sensory nerve activation and epigenetic regulation via DNA methylation and histone modifications are crucial in allergic responses.

Purpose of the Study:

  • To elucidate the complex cellular and molecular mechanisms underlying allergic inflammation.
  • To identify key transcription factors and epigenetic regulators involved in allergic responses.
  • To explore the challenges and potential of developing novel therapeutic targets for allergic diseases.

Main Methods:

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Humanized Mediator Release Assay as a Read-Out for Allergen Potency
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Humanized Mediator Release Assay as a Read-Out for Allergen Potency

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Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
11:54

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples

Published on: January 21, 2018

Related Experiment Videos

Last Updated: May 31, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

Humanized Mediator Release Assay as a Read-Out for Allergen Potency
10:22

Humanized Mediator Release Assay as a Read-Out for Allergen Potency

Published on: June 29, 2021

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
11:54

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples

Published on: January 21, 2018

  • Review of current literature on the pathophysiology of allergic inflammation.
  • Analysis of the roles of inflammatory cells, mediators, and signaling pathways.
  • Examination of transcription factors (e.g., NF-κB, GATA3) and epigenetic mechanisms.

Main Results:

  • Allergic inflammation is characterized by a multi-faceted interplay of immune cells and mediators.
  • Transcription factors like NF-κB and GATA3, alongside epigenetic modifications, orchestrate inflammatory gene expression.
  • Endogenous anti-inflammatory mechanisms can be defective, perpetuating allergic inflammation.

Conclusions:

  • A comprehensive understanding of allergic inflammation pathophysiology reveals numerous therapeutic targets.
  • Developing novel therapies remains challenging, though corticosteroids demonstrate broad efficacy, including epigenetic modulation.
  • Further research into these pathways may lead to more effective treatments for allergic conditions.