Related Experiment Video
Updated: Aug 26, 2026
Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Regulation of ICAM-1 expression in mouse macrophages
1Department of Pharmaceutical Sciences, University of Connecticut, Storrs 06269, USA.
Abstract:
In a mouse model of silica (SI) induced lung injury, SI exposure increases expression of intercellular adhesion molecule-1 (ICAM-1) on lung (alveolar/interstitial) macrophages and alveolar type II epithelial cells. To investigate the regulation of SI induced ICAM-1 expression on mouse macrophages, freshly isolated macrophages (alveolar, peritoneal) and macrophage cell lines (MH-S, RAW 264.7) were evaluated for ICAM-1 expression elicited by the particle silica (alpha quartz; 20 microg/ml; 6 microg/cm2) or the inflammatory cytokine, TNFalpha (20 ng/ml). TNFalpha significantly increased ICAM-1 expression in all cell types whereas SI elicited an increase in peritoneal macrophages (PM) and the cell line, MH-S. This pattern of increased expression was confirmed by immunocytochemistry. To investigate the regulation of ICAM-1 expression, PM were incubated with SI, TNFalpha or media concomitantly with anti-TNFalpha antibody, the antioxidant, NAC, or the iNOS synthase inhibitor, L-NAME. Both anti-TNFalpha and NAC, but not L-NAME, inhibited elicited (TNFalpha, SI) as well as constitutive (media) ICAM-1 expression. These data demonstrate that both inflammatory cytokines and inorganic particles can increase ICAM-1 expression on mouse macrophages and that this expression is mediated, in part, by TNFalpha and reactive oxygen species.
Insights
Silica particles and TNFalpha increase intercellular adhesion molecule-1 (ICAM-1) on mouse macrophages. This expression is partly regulated by TNFalpha and reactive oxygen species, impacting lung injury.
Area of Science:
- Immunology
- Toxicology
- Cell Biology
Background:
- Silica (SI) exposure causes lung injury by increasing intercellular adhesion molecule-1 (ICAM-1) on lung cells.
- Understanding ICAM-1 regulation on macrophages is crucial for addressing silica-induced lung inflammation.
Purpose of the Study:
- To investigate the regulation of silica-induced ICAM-1 expression on mouse macrophages.
- To determine the roles of TNFalpha and reactive oxygen species in this process.
Main Methods:
- Macrophages (primary and cell lines) were exposed to silica particles or TNFalpha.
- Immunocytochemistry was used to confirm ICAM-1 expression.
- Inhibition studies involved anti-TNFalpha antibody, N-acetylcysteine (NAC), and L-NAME.
Main Results:
- TNFalpha increased ICAM-1 in all tested macrophage types.
- Silica increased ICAM-1 in peritoneal macrophages and the MH-S cell line.
- Anti-TNFalpha and NAC significantly inhibited ICAM-1 expression, while L-NAME did not.
Conclusions:
- Both inflammatory cytokines and inorganic particles like silica upregulate macrophage ICAM-1.
- TNFalpha and reactive oxygen species partially mediate silica-induced ICAM-1 expression.
- Targeting TNFalpha and oxidative stress may mitigate silica-induced lung inflammation.
