Abstract
Patients with septic shock by multidrug resistant microorganisms (MDR) are a specific sepsis population with a high mortality risk. The exposure to an initial inappropriate empiric antibiotic therapy has been considered responsible for the increased mortality, although other factors such as immune-paralysis seem to play a pivotal role. Therefore, beyond conventional early antibiotic therapy and fluid resuscitation, this population may benefit from the use of alternative strategies aimed at supporting the immune system. In this review we present an overview of the relationship between MDR infections and immune response and focus on the rationale and the clinical data available on the possible adjunctive immunotherapies, including blood purification techniques and different pharmacological approaches.
Highlights
Since early 90s, the American College of Chest Physicians and Society of Critical Care Medicine Consensus Conference has placed great emphasis to sepsis and its definition [1]
In this review we present an overview of the relationship between multidrug resistant (MDR) infections and immune response and focus on the rationale and the clinical data available on the possible adjunctive immunotherapies, including blood purification techniques and different pharmacological approaches
A complex system of intracellular signals is created by the binding of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) that lead to the expression of several common gene classes involved in inflammation, adaptive immunity, and cellular metabolism [3]
Summary
Since early 90s, the American College of Chest Physicians and Society of Critical Care Medicine Consensus Conference has placed great emphasis to sepsis and its definition [1]. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) revised the definitions emphasizing the role of the host response and the related pathophysiological mechanisms inducing organ dysfunction [2]. The change of perspective from invading pathogens to the host response has radically transformed the vision of sepsis pathobiology in the last decades. A complex system of intracellular signals is created by the binding of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) that lead to the expression of several common gene classes involved in inflammation, adaptive immunity, and cellular metabolism [3]. The recognition of PAMPs and DAMPs produces the recruitment of proinflammatory intermediates that initiate the expression of early activation genes [4]
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