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Asthma I: Introduction

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...

Asthma-II: Pathophysiology and Classification

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:

Asthma: Pathogenesis and Management

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-I: Introduction

Asthma-I: Introduction

Asthma is a chronic respiratory ailment that requires careful management due to its varying symptoms and influencing factors. It is characterized by airway inflammation, bronchial hyperresponsiveness, and reversible airflow obstruction, leading to symptoms like wheezing, shortness of breath, chest tightness, and coughing. The symptom frequency and intensity may vary considerably over time. It is also linked to immune system responses to allergens and irritants, highlighting the complex...

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...

Asthma III: Clinical Manifestations

Asthma III: Clinical Manifestations

Asthma presents with a characteristic pattern of episodic respiratory symptoms that reflect underlying airway inflammation, bronchoconstriction, and mucus hypersecretion. Although severity varies among individuals, certain clinical manifestations are considered hallmarks of the disorder and often guide diagnosis and assessment.Respiratory SymptomsA persistent cough is one of the most common early features of asthma. It is frequently dry and tends to worsen at night or in the early morning,...

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Related Experiment Video

Updated: Jun 18, 2026

Cultivate Primary Nasal Epithelial Cells from Children and Reprogram into Induced Pluripotent Stem Cells

Cultivate Primary Nasal Epithelial Cells from Children and Reprogram into Induced Pluripotent Stem Cells

Published on: March 10, 2016

Epigenetic changes in childhood asthma.

Rakesh K Kumar¹, Megan P Hitchins, Paul S Foster

¹Department of Pathology, University of New South Wales, Sydney NSW, Australia. r.kumar@unsw.edu.au

Disease Models & Mechanisms

|November 7, 2009

Summary

This summary is machine-generated.

Epigenetic changes may explain how environmental factors like viral infections and allergens contribute to childhood asthma development and its T helper 2 immune response. Understanding these mechanisms offers new prevention and treatment strategies.

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Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

Published on: August 7, 2017

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Last Updated: Jun 18, 2026

Cultivate Primary Nasal Epithelial Cells from Children and Reprogram into Induced Pluripotent Stem Cells

Cultivate Primary Nasal Epithelial Cells from Children and Reprogram into Induced Pluripotent Stem Cells

Published on: March 10, 2016

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

Published on: August 7, 2017

Area of Science:

Immunology
Environmental Health
Genetics

Background:

Childhood asthma is associated with atopy and a T helper 2 (Th2)-polarized immune response.
Severe viral respiratory infections and allergen exposure in early life are implicated as synergistic factors in asthma development.
The mechanisms by which environmental factors induce stable phenotypic alterations are not fully understood.

Purpose of the Study:

To explore the role of epigenetic mechanisms in the development and maintenance of Th2 responses in childhood asthma.
To investigate the contribution of epigenetic modifications to altered microRNA gene expression in asthmatic airway inflammation.

Main Methods:

This study reviews current understanding of epigenetic mechanisms in asthma.
It synthesizes evidence linking environmental exposures to epigenetic alterations and Th2 polarization.
The role of microRNAs in asthma pathogenesis is discussed in the context of epigenetics.

Main Results:

Epigenetic changes are recognized as a potential basis for establishing and maintaining Th2 responses in asthma.
Alterations in regulatory microRNA gene expression profiles may drive ongoing airway inflammation in asthma.
Epigenetic mechanisms likely play a significant role in both the development and persistence of asthma.

Conclusions:

Understanding epigenetic mechanisms in childhood asthma is crucial.
This knowledge has the potential to uncover novel strategies for primary prevention and therapeutic intervention.
Targeting epigenetic pathways may offer new avenues for managing childhood asthma.