When friend turns foe: central and peripheral neuroinflammation in central nervous system injury

Abstract

Injury to the central nervous system (CNS) is common, and though it has been well studied, many aspects of traumatic brain injury (TBI) and stroke are poorly understood. TBI and stroke are two pathologic events that can cause severe, immediate impact to the neurostructure and function of the CNS, which has been recognized recently to be exacerbated by the body's own immune response. Although the brain damage induced by the initial trauma is most likely unsalvageable, the secondary immunologic deterioration of neural tissue gives ample opportunity for therapeutic strategists seeking to mitigate TBI's secondary detrimental effects. The purpose of this paper is to highlight the cell death mechanisms associated with CNS injury with special emphasis on inflammation. The authors discuss sources of inflammation, and introduce the role of the spleen in the systemic response to inflammation after CNS injury.

Keywords: Head trauma; central nervous system; inflammatory response; secondary cell death; spleen; systemic.

Figure 1

Central and peripheral sources of inflammation. Following CNS injury, such as stroke and TBI, the traditional concept entails a robust inflammatory response within the brain, but equally compelling recent evidence has demonstrated an active inflammatory response, especially from the spleen, contributing to the progression of the disease. Together with other secondary cell death factors, both central and peripheral inflammation exacerbate CNS injury. CNS: central nervous system; TBI: traumatic brain injury