The response of the host microcirculation to bacterial sepsis: does the pathogen matter?

Abstract

Sepsis results from the interaction between a host and an invading pathogen. The microcirculatory dysfunction is now considered central in the development of the often deadly multiple organ dysfunction syndrome in septic shock patients. The microcirculatory flow shutdown and flow shunting leading to oxygen demand and supply mismatch at the cellular level and the local activation of inflammatory pathways resulting from the leukocyte-endothelium interactions are both features of the sepsis-induced microcirculatory dysfunction. Although the host response through the inflammatory and immunologic response appears to be critical, there are also evidences that Gram-positive and Gram-negative bacteria can exert different effects at the microcirculatory level. In this review we discuss available data on the potential bacterial-specific microcirculatory alterations observed during sepsis.

Fig. 1

Proposed Mechanisms of the role of microcirculatory alterations in sepsis-related multiple organ failure. Recognition of bacterial products by pattern-recognition receptor (PRR) on immune and endothelial cells initiate host responses at the microcirculatory level leading to endothelial cells damage, leukocytes activation and adhesion, and production of reactive oxygen species (ROS). Microcirculatory flow shutdown will follow due to microthrombi, interstitial edema, and alteration of vascular tone