Related Experiment Video

Updated: May 13, 2026

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
08:54

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure

Published on: October 22, 2019

Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD

Jun Kojima1, Jun Araya, Hiromichi Hara

  • 1Department of Internal Medicine, Division of Respiratory Diseases, Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo 105-8461, Japan.

Respiratory Research
|March 19, 2013
PubMed
Abstract

Insights

Apoptosis inhibitor of macrophage (AIM) accumulates in chronic obstructive pulmonary disease (COPD) lungs, particularly in alveolar macrophages (AM) exposed to cigarette smoke. AIM contributes to AM survival, potentially driving COPD pathogenesis.

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Cell Biology

Background:

  • Alveolar macrophages (AM) accumulation, driven by apoptosis resistance, is linked to chronic obstructive pulmonary disease (COPD) pathogenesis.
  • Apoptosis inhibitor of macrophage (AIM) is produced by macrophages and exhibits anti-apoptotic properties.

Purpose of the Study:

  • To investigate AIM expression in AM from COPD patients.
  • To determine AIM's role in regulating AM apoptosis following cigarette smoke extract (CSE) exposure.

Main Methods:

  • Immunohistochemistry to quantify AIM-positive AM in control, non-COPD smoker, and COPD lung tissues.
  • Isolation and culture of AM from bronchoalveolar lavage fluid (BALF) for AIM expression analysis.
  • Evaluation of AIM's effect on Bcl-xL expression and apoptosis in U937 cells exposed to CSE.

Main Results:

  • COPD lungs showed significantly increased numbers of AM and AIM-positive AM.
  • AIM expression (mRNA and protein) in AM increased with CSE exposure.
  • AIM elevated Bcl-xL expression in AM, contributing to CSE-induced apoptosis resistance.

Conclusions:

  • AIM expression is elevated in COPD lungs and associated with cigarette smoking.
  • AIM may contribute to AM accumulation in COPD by inhibiting apoptosis.

More Related Videos

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages09:09

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

Published on: April 20, 2018

Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice11:20

Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice

Published on: March 2, 2019

Related Concept Videos

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.
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...