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Related Concept Videos

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

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 III: Chronic Bronchitis Features01:24

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...
Obesity01:24

Obesity

The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in adipocytes...
Chronic Obstructive Pulmonary Disease I: Introduction01:23

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: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

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-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:

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Related Experiment Video

Updated: Jul 2, 2026

Intraperitoneal Glucose Tolerance Test, Measurement of Lung Function, and Fixation of the Lung to Study the Impact of Obesity and Impaired Metabolism on Pulmonary Outcomes
08:30

Intraperitoneal Glucose Tolerance Test, Measurement of Lung Function, and Fixation of the Lung to Study the Impact of Obesity and Impaired Metabolism on Pulmonary Outcomes

Published on: March 15, 2018

Obesity Promotes Lung Carcinogenesis Through Airway Immune Dysfunction.

Joseph Barbi1, Randall J Smith1, Yeshwanth R Vedire2

  • 1Department of Thoracic Surgery, Roswell Park Comprehensive Cancer Center, Buffalo, New York, 14263, USA; Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, New York, 14263, USA.

Journal of Thoracic Oncology : Official Publication of the International Association for the Study of Lung Cancer
|June 30, 2026
PubMed
Summary

High abdominal fat area is linked to increased lung cancer risk and immune suppression. Obesity enhances lung carcinogenesis by upregulating immune suppressive mechanisms, challenging the obesity paradox theory.

Keywords:
Carcinogenesisimmune suppressionlungobesity

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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

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Last Updated: Jul 2, 2026

Intraperitoneal Glucose Tolerance Test, Measurement of Lung Function, and Fixation of the Lung to Study the Impact of Obesity and Impaired Metabolism on Pulmonary Outcomes
08:30

Intraperitoneal Glucose Tolerance Test, Measurement of Lung Function, and Fixation of the Lung to Study the Impact of Obesity and Impaired Metabolism on Pulmonary Outcomes

Published on: March 15, 2018

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

Area of Science:

  • Oncology
  • Immunology
  • Metabolic Disease

Background:

  • Obesity is linked to immune dysfunction, yet paradoxically associated with decreased lung cancer risk.
  • This phenomenon, known as the "Obesity Paradox," requires further investigation for mechanistic clarity.

Purpose of the Study:

  • To investigate the relationship between obesity and lung cancer risk.
  • To elucidate the underlying immunological mechanisms contributing to this association.

Main Methods:

  • A case-control study analyzed lung cancer risk in relation to total abdominal fat area (TFA) using CT scans.
  • Gene expression, immune cell profiling (flow cytometry), and preclinical models of lung carcinogenesis were employed.
  • Analysis included airway gene expression, broncho-alveolar lavage, and murine lung immune contexture.

Main Results:

  • Higher TFA was significantly associated with increased lung cancer risk in both univariate and multivariable analyses.
  • Obesity was linked to suppressed immune activity in airways, characterized by increased regulatory T cells (Tregs) and myeloid cells.
  • Preclinical models demonstrated that obesity exacerbates lung carcinogenesis, with obesity-enhanced Tregs promoting tumor growth and compromised immune surveillance.

Conclusions:

  • Obesity is associated with enhanced lung carcinogenesis, contrary to the "Obesity Paradox".
  • Immune suppression, driven by activated Tregs and other mechanisms, is upregulated in obesity and contributes to increased lung cancer risk.
  • These findings highlight the detrimental role of obesity in lung cancer development and challenge existing paradigms.