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.
(c) 2009 Elsevier Inc. All rights reserved.