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Macrophages and inflammatory mediators in tissue injury
1Department of Pharmacology and Toxicology, Rutgers University, Piscataway, New Jersey 08855-0789, USA.
Annual Review of Pharmacology and Toxicology
|January 1, 1995
Summary
Xenobiotics can harm tissues directly or indirectly by activating macrophages. These immune cells release mediators that contribute to tissue damage, a process observed in the lungs and liver.
Area of Science:
- Toxicology
- Immunology
- Cell Biology
Background:
- Xenobiotics cause tissue injury through direct and indirect mechanisms.
- Indirect injury involves the recruitment and activation of tissue macrophages.
- Macrophages release various mediators implicated in tissue damage.
Purpose of the Study:
- To investigate the role of macrophages and their mediators in xenobiotic-induced tissue injury.
- To determine if blocking macrophage function reduces xenobiotic-induced tissue damage.
Main Methods:
- Review of existing literature on xenobiotic toxicity and macrophage activation.
- Analysis of studies investigating macrophage mediator release in lung and liver injury models.
- Examination of data from experiments where macrophage function was inhibited.
Main Results:
- Xenobiotics induce macrophage accumulation and mediator release in target tissues.
- Blocking macrophage function reduces injury caused by agents like ozone, bleomycin, acetaminophen, carbon tetrachloride, and galactosamine.
- Macrophages release cytotoxic cytokines, reactive oxygen species, and nitric oxide, contributing to pathogenesis.
Conclusions:
- Macrophages and their released mediators play a significant role in xenobiotic-induced tissue injury.
- Targeting macrophage activation presents a potential therapeutic strategy for mitigating xenobiotic toxicity.