Role of LPS tolerance in experimental septic oxidative stress

Abstract

Sepsis is known as a systemic inflammatory syndrome in response to an infection. It is a serious illness which can cause multiple organ failure and is currently the leading cause of death in patients admitted to Intensive Care Unit. Infection by gram-negative bacteria represents most of the recorded cases of Sepsis. The lipopolysaccharide (LPS) of the bacterial outer membrane component initiates a cascade of activities of the human immune system. A response to LPS produces numerous inflammatory mediators and induces the release of reactive oxygen species (ROS) capable of causing an oxidative stress. A high production of ROS leads to cell dysfunction, affecting the genome, the organelles and cell membranes. The negative impact of the disease can be lessened by the host's ability to tolerate the presence of pathogens. It is known that a prior exposure to the LPS alters the pattern of gene expression of inflammatory cytokines. The tolerance to LPS is related to a reduced production and release of cytokines from phagocytes in re-exposure to LPS, in order to reduce negative impacts of exceeded activation of the immune system. (AU)