Fig. 8

Traumatic injury mediated disruption of immune homeostasis and a prematurely aged immune phenotype. Trauma-induced development of systemic inflammatory response (SIRS) in trauma patients as early as 3 days post hospitalisation which persists and a compensatory anti-inflammatory (IL10) which peaks 14 days post hospitalisation. Traumatic injury induces T cell lymphopenia, with a maximum drop in systemic T cells observed 14 days post hospitalisation which persists two months later. Furthermore, trauma-induced activation of the HPA axis resulting in elevated systemic cortisol levels and systemic inflammation (elevated IL6 levels) have been associated with thymic involution in these patients, resulting in a reduced thymic output of naïve T cells. Other changes in T cell subset distribution include; elevated systemic memory T cells and inflammatory senescent T cells correlating with systemic levels of TNFα. An expansion of regulatory T cells occurs in traumatic injury patients that has been associated with elevated systemic IL10 levels. Similar to T cells, a drop in naïve B cells and accumulation of switched memory B cells occurs post-trauma which persists two months later. Trauma-triggered T cell lymphopenia, loss of naïve T cells, accumulation of memory and pro-inflammatory cytokines have been identified as predictive markers for sepsis in trauma patients