Macrophages and tissue injury: Agents of defense or destruction?

Debra L. Laskin, Vasanthi R. Sunil, Carol R. Gardner, Jeffrey D. Laskin

Research output: Contribution to journalArticlepeer-review

303 Scopus citations


The past several years have seen the accumulation of evidence demonstrating that tissue injury induced by diverse toxicants is due not only to their direct effects on target tissues but also indirectly to the actions of resident and infiltrating macrophages. These cells release an array of mediators with cytotoxic, pro- and anti-inflammatory, angiogenic, fibrogenic, and mitogenic activity, which function to fight infections, limit tissue injury, and promote wound healing. However, following exposure to toxicants, macrophages can become hyperresponsive, resulting in uncontrolled or dysregulated release of mediators that exacerbate acute tissue injury and/or promote the development of chronic diseases such as fibrosis and cancer. Evidence suggests that the diverse activity of macrophages is mediated by distinct subpopulations that develop in response to signals within their microenvironment. Understanding the precise roles of these different macrophage populations in the pathogenic response to toxicants is key to designing effective treatments for minimizing tissue damage and chronic disease and for facilitating wound repair.

Original languageEnglish (US)
Pages (from-to)267-288
Number of pages22
JournalAnnual Review of Pharmacology and Toxicology
StatePublished - Feb 10 2011

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology


  • RNS
  • ROS
  • cytokines
  • fibrosis
  • inflammation
  • liver
  • lung

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