Animal models of neuroinflammation secondary to acute insults originated outside the brain

Abstract

The term ""neuroinflammation"" has been widely used to describe a series of acute or chronic conditions that cause inflammation in the central nervous system (CNS). Neurological damage can be a consequence of direct local injury or, secondary, of systemic or even distant inflammatory processes. In this respect, animal models have been developed to better understand the pathophysiology and, possibly, to evaluate more effective methods of treatment for these disorders. Animal models that promote alterations in blood-brain barrier permeability-the activation of microglia or astrocytes, modifications in neuropeptide expression, oxidative stress, increased apoptosis, release of inflammatory mediators, leukocyte infiltration, and brain edema-are likely to involve neuroinflammation and therefore can serve as useful models for human inflammatory CNS injury. This review describes the major animal models of neuroinflammation triggered by systemic or distant inflammatory processes. We will focus on animal models of acute neurologic damage; experimental models that lead to chronic neuroinflammation will not be addressed here.