Linking oxidative stress to inflammation: Toll-like receptors

Roop Gill*, Allan Tsung, Timothy Billiar

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

449 Scopus citations


Injury caused by oxidative stress occurs in many clinical scenarios involving ischemia and reperfusion such as organ transplantation, hemorrhagic shock (HS), myocardial infarction, and cerebral vascular accidents. Activation of the immune system as a result of disturbances in the redox state of cells seems to contribute to tissue and organ damage in these conditions. The link between oxidative stress and inflammatory pathways is poorly understood. Recently, Toll-like receptors (TLRs) have been shown to mediate the inflammatory response seen in experimental ischemia and reperfusion (I/R). The TLR family of receptors involved in alerting the innate immune system of danger seems to be activated by damage-associated molecular pattern molecules (DAMPs) that are released during conditions of oxidative stress. In this review, we examine the role of TLRs in various experimental models of oxidative stress such as HS and I/R. We also report on potential DAMPs that may interact with TLRs in mediating injury. Finally, potential mechanisms by which reactive oxygen species from NADPH oxidase can signal the commencement of inflammatory pathways through TLRs are explored.

Original languageEnglish
Pages (from-to)1121-1132
Number of pages12
JournalFree Radical Biology and Medicine
Issue number9
StatePublished - May 2010
Externally publishedYes


  • DAMPs
  • Free radicals
  • HMGB1
  • Hemorrhagic shock
  • Ischemia/reperfusion
  • NADPH oxidase
  • Redox stress
  • Toll-like receptor


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