Cytokine Gene Polymorphism and Sepsis

Abstract

Trauma is a significant problem across the globe with mortality more than 50%. Despite the advancement of pre-hospital care to trauma patients, early resuscitation in the emergency department, surgical interventions and intensive care monitoring mortality rate has not improved yet. The higher rate of mortality in trauma patients is usually associated with development of complications such as sepsis, septic shock, and MOF which may occur due to hysterical immune inflammatory responses. Trauma patients who developed these complications in the ICU have comparatively higher chances of mortality. Cytokines are very important for host immune response against infections and play vital roles in the regulation of innate and adaptive immunity. The slanted expression of cytokines due to trauma may be involved in development of sepsis and related complications. The recently published work from various studies suggested that slanted expression of cytokines correlates with the variations in the promoter and structural regions of cytokine genes, which may be responsible for inter-individual differences in susceptibility to sepsis. Therefore, understanding the variations in cytokine genes and associated outcomes due to trauma would possibly contribute to the event of latest genetically changed diagnostic and therapeutic interventions that will improve the outcome in post-traumatic sepsis patients.

Systemic T Cell Exhaustion Dynamics Is Linked to Early High Mobility Group Box Protein 1 (HMGB1) Driven Hyper-Inflammation in a Polytrauma Rat Model

“…In the case of trauma hemorrhage patients, a study demonstrated that Th type 1 cell (Th1) responses (secrete IL-2, IFNγ) were suppressed. In contrast, the Th type 2 (Th2) responses (secrete IL-4, IL-5, IL-13 and IL-10) were elevated, leading to a suppressed adaptive immune response and increased susceptibility to sepsis [ 35 ]. Findings from another group indicate that following severe burn trauma, a notable increase in Th2 response occurs without altering the Th1 response [ 36 , 37 ].…”