Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

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...

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 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 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,...

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

The Duffy antigen receptor for chemokines regulates asthma pathophysiology.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2017

Same author

Genome-wide association study of leukotriene modifier response in asthma.

The pharmacogenomics journal·2015

Same author

Mechanisms of airway hyper-responsiveness in asthma: the past, present and yet to come.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2015

Same author

A genome-wide association study of bronchodilator response in asthmatics.

The pharmacogenomics journal·2013

Same author

HLA-DQ strikes again: genome-wide association study further confirms HLA-DQ in the diagnosis of asthma among adults.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2012

Same author

A polymorphism in the thyroid hormone receptor gene is associated with bronchodilator response in asthmatics.

The pharmacogenomics journal·2012

Search research articles

Related Experiment Video

Updated: May 7, 2026

Murine Model of Allergen Induced Asthma

Murine Model of Allergen Induced Asthma

Published on: May 14, 2012

Sinusitis and asthma: an animal model.

¹Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colo.

The Journal of Allergy and Clinical Immunology

|September 1, 1992

Summary

This summary is machine-generated.

Complement-induced maxillary sinusitis in rabbits caused lower airways hyperresponsiveness, likely due to inflammatory mediators from postnasal drip. This suggests upper airway inflammation can impact lower airways without cell migration.

More Related Videos

Studying Microbial Communities In Vivo: A Model of Host-mediated Interaction Between Candida Albicans and Pseudomonas Aeruginosa in the Airways

Studying Microbial Communities In Vivo: A Model of Host-mediated Interaction Between Candida Albicans and Pseudomonas Aeruginosa in the Airways

Published on: January 13, 2016

Acupuncture in a Rat Model of Asthma

Acupuncture in a Rat Model of Asthma

Published on: August 25, 2020

Related Experiment Videos

Last Updated: May 7, 2026

Murine Model of Allergen Induced Asthma

Murine Model of Allergen Induced Asthma

Published on: May 14, 2012

Studying Microbial Communities In Vivo: A Model of Host-mediated Interaction Between Candida Albicans and Pseudomonas Aeruginosa in the Airways

Studying Microbial Communities In Vivo: A Model of Host-mediated Interaction Between Candida Albicans and Pseudomonas Aeruginosa in the Airways

Published on: January 13, 2016

Acupuncture in a Rat Model of Asthma

Acupuncture in a Rat Model of Asthma

Published on: August 25, 2020

Area of Science:

Immunology
Respiratory Medicine
Otolaryngology

Background:

Upper and lower airway diseases frequently coexist clinically.
The mechanisms linking upper airway inflammation to lower airway dysfunction are not fully understood.

Purpose of the Study:

To investigate the link between upper airway inflammation (maxillary sinusitis) and lower airway hyperresponsiveness.
To elucidate the potential mechanisms involved in this association.

Main Methods:

An animal model was developed using rabbits with complement-induced maxillary sinusitis.
Histamine-induced lower airways hyperresponsiveness was measured.
Potential mechanisms including postnasal drip, blood-borne mediators, and nasobronchial reflexes were evaluated.

Main Results:

Complement-induced maxillary sinusitis led to nonspecific lower airways hyperresponsiveness to inhaled histamine.
The primary mechanism identified was the direct passage of inflammatory mediators from the upper to the lower respiratory tract (postnasal drip).
Other potential mechanisms, such as blood-borne mediators or cell migration, were not supported by the findings.

Conclusions:

Inflammatory mediators from upper airway inflammation can cause lower airways dysfunction.
This pathway may explain the clinical association between sinusitis and asthma.
Airways dysfunction can occur due to inflammation without direct cell migration into the airways.