ABSTRACT
The brain is a complex organization of specialized cells responsible for controlling the function of an entire organism. As such, this highly regulated system must be able to quickly respond to a number of potential pathological states including ischemia, injury or infection to mediate damage and promote repair (Dheen et al., 2007). This response involves the upregulation of numerous proteins associated with neuroinfl ammation, referred to as “sterile infl ammation” when it occurs in the absence of pathogen (Chen and Nunez, 2010). Neuroinfl ammation following injury begins with the release of Damage-Associated Molecular Patterns (DAMPs) from dead cells. Recognition of these molecular patterns by pattern recognition receptors on Central Nervous System (CNS) glial cells begins the infl ammatory cascade (Berda-Haddad et al., 2011). Pattern recognition receptors are primarily found on astrocytes and reactive microglia; their activation initiates the expression of infl ammation-related proteins to recruit and activate more glial cells and peripheral immune cells to the site of injury (Suffredini et al., 1999). In addition, endothelial cells, neurons and infi ltrating leukocytes can also produce inflammation-related proteins, generally described
1 US Army Medical Research Institute of Chemical Defense, Research Division/ Pharmacology Branch, 3100 Ricketts Point, Aberdeen Proving Ground, MD 21010.
