*Pathophysiological Changes and Systemic Inflammation in Brain Dead Organ Donors… DOI: http://dx.doi.org/10.5772/intechopen.94360*

The up-regulated expression of cell adhesion molecules (CAMs), including selectines, vascular (VCAM-1) and intracellular CAMs (ICAM-1) on the endothelium of potential grafts plays a critical role in numerous inflammatory processes. One of their tasks is the recruitment of circulating monocytes, macrophages and polymorphonuclear leukocytes as shown in organ biopsies after organ retrieval [12, 16, 21, 22]. Therefore, unsurprisingly, increased levels of CAMs have been associated with increased mortality in transplant recipients [16].

The activation of leukocyte populations in peripheral organs further maintains an inflammatory environment by expressing CAMs and releasing proinflammatory substances, among others, tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) [16]. Especially IFN-γ induces the expression of major histocompatibility complex (MHC) classes I and II on graft cells, which potentiate the immunogenicity of organs via the T-cell recognition process. The activated organs provoke a host immune system after engraftment, resulting in severe acute or chronic rejection [23].

Complement activation has already been demonstrated in ischemia–reperfusion injury and rejection. Fragments of complement activation products have been measured in plasma and organ biopsies. Their values were higher compared to living donors [24–26].
