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Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

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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...

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation

Chronic Obstructive Pulmonary Disease II: Emphysema

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Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.

Asthma I: Introduction

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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...

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Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting respiratory condition requiring continuous attention and care. It is a progressive lung disease that leads to breathing challenges due to airflow obstruction. It manifests as persistent respiratory symptoms and restricted airflow resulting from abnormalities in the airways and alveoli, usually due to long-term exposure to harmful particles or gases. COPD mainly consists of two primary conditions: emphysema and chronic bronchitis.

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Updated: Jul 5, 2026

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters

Published on: July 12, 2024

Particulate matter exposure induces persistent lung inflammation and endothelial dysfunction.

Eiji Tamagawa¹, Ni Bai, Kiyoshi Morimoto

¹Division of Respiratory Medicine, University of British Columbia and James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul's Hospital, Vancouver, British Columbia, Canada.

American Journal of Physiology. Lung Cellular and Molecular Physiology

|May 13, 2008

Summary

Particulate matter air pollution (PM) exposure causes lung and systemic inflammation, leading to vascular endothelial dysfunction. This study demonstrates PM exposure

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Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Published on: December 10, 2021

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Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters

Published on: July 12, 2024

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Published on: December 10, 2021

Area of Science:

Environmental Health
Cardiovascular Disease
Toxicology

Background:

Epidemiologic and animal studies link particulate matter (PM) air pollution to atherosclerosis.
The role of PM-induced lung and systemic inflammation in this process remains unclear.

Purpose of the Study:

To investigate if PM exposure induces lung and systemic inflammation, contributing to vascular endothelial dysfunction.
To determine the association between PM-induced inflammation and atherosclerosis development.

Main Methods:

New Zealand White rabbits were exposed to PM smaller than 10 micrometers (PM10) or saline intratracheally for acute (5 days) and chronic (4 weeks) periods.
Lung inflammation was assessed via morphometry; systemic inflammation by blood cell counts and serum cytokine levels (IL-6).
Vascular endothelial function was evaluated by responses to acetylcholine (ACh) and sodium nitroprusside (SNP).

Main Results:

PM10 exposure significantly increased lung macrophages and activated macrophages.
Acute PM10 exposure elevated serum IL-6 levels, correlating with lung inflammation and reduced ACh-induced arterial relaxation.
Both acute and chronic PM10 exposure impaired endothelial-dependent vasodilation (ACh) but not endothelial-independent vasodilation (SNP).

Conclusions:

PM10 exposure triggers lung and systemic inflammation in rabbits.
This inflammation is associated with vascular endothelial dysfunction, a critical factor in atherosclerosis.
PM-induced inflammatory responses may contribute to adverse vascular events linked to air pollution exposure.