Related Experiment Video

Updated: Sep 30, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Silica-induced apoptosis in murine macrophage: involvement of tumor necrosis factor-alpha and nuclear factor-kappaB

Evelyne Gozal1, Luis A Ortiz, Xiaoyan Zou

  • 1Section of Pulmonary Diseases, Critical Care, Tulane-Xavier Center for Bioenvironmental Research, Tulane University Medical Center, New Orleans, Louisiana, USA. evelyne.gozal@louisville.edu

American Journal of Respiratory Cell and Molecular Biology
|July 2, 2002
PubMed

Insights

Silica exposure triggers tumor necrosis factor-alpha release and nuclear factor-kappaB activation in macrophages, contributing to lung fibrosis. Macrophage responses to silica vary, with nuclear factor-kappaB playing dual apoptotic roles.

Area of Science:

  • Immunology
  • Cell Biology
  • Toxicology

Background:

  • Alveolar macrophages are crucial in silica-induced lung fibrosis.
  • Silica exposure stimulates tumor necrosis factor-alpha (TNF-α) release and nuclear factor-kappaB (NF-κB) activation.
  • Apoptosis is implicated in silica-induced lung pathogenesis.

Purpose of the Study:

  • To investigate the relationship between TNF-α, NF-κB, and apoptosis in silica-exposed murine macrophage cell lines.
  • To compare the sensitivity and responses of RAW 264.7 and IC-21 macrophage cell lines to silica.

Main Methods:

  • Exposure of RAW 264.7 and IC-21 macrophage cell lines to silica (0.2 or 1 mg/ml for 6 h).
  • Assessment of apoptosis, TNF-α production, and NF-κB activation.
  • Inhibition of NF-κB using BAY11-7082.
  • Stimulation with lipopolysaccharide (LPS) to compare responses.

Main Results:

  • RAW 264.7 cells showed higher sensitivity to silica, with increased apoptosis, TNF-α production, and NF-κB activation compared to IC-21 cells.
  • NF-κB inhibition in RAW 264.7 cells enhanced apoptosis and reduced TNF-α release.
  • Silica induced apoptosis independently of TNF-α in IC-21 cells.
  • LPS induced TNF-α and NF-κB activation in both cell lines, with NF-κB inhibition reducing TNF-α release.

Conclusions:

  • TNF-α induction is dependent on NF-κB activation in both macrophage cell lines.
  • Silica can induce apoptosis in murine macrophages independently of TNF-α.
  • NF-κB activation in macrophages may have dual pro- and anti-apoptotic roles in silica injury.

More Related Videos

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition06:12

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Published on: March 3, 2023

Related Concept Videos

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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.