The sepsis induced defective aggravation of immune cells: a translational science underling chemico-biological interactions from altered bioenergetics and/or cellular metabolism to organ dysfunction.

Sepsis is described as a systemic immune response of the body to an infectious process that might result in dysfunctional organs that may lead to death. In clinical practice, sepsis is considered a medical emergency. The initial event in sepsis caused by a deregulated host response towards harmful microorganisms that leads to an aggravated systemic inflammatory response syndrome (SIRS) to tackle with pathogen invasion and a compensatory anti-inflammatory response syndrome (CARS) that lasts for several days. The inflammatory response and the cellular damage as well as the risk of an organ dysfunction are in direct proportion. Even though, the pathogenesis of sepsis remains unclear, many studies have shown evidence of role of oxidants and antioxidants in sepsis. The altered innate and adaptive immune cell and upregulated production and release of cytokines and chemokines most probably due to involvement of JAK-STAT pathway, disturbance in redox homeostasis due to low clearance of lactate and other oxidative stressors, contributes to sepsis process to organ dysfunction which contribute to increase rates of mortality among these patients. Hence, the treatment strategies for sepsis include antibiotics, ventilator and blood glucose management and other strategies for resuscitation are rapidly progressing. In the current review, we mainly concentrate on throwing light on the main molecular aspects and chemico-biological interactions that shows involvement in pathways manipulating alteration in physiology of immune cells (innate and adaptive) that change the bioenergetics/cellular metabolism to organ dysfunction and correlation of these altered pathway, improve the understating for new therapeutic target for sepsis.