Innate immunity and inflammation: The molecular mechanisms governing the cross-talk between innate immune and endothelial cells

Abstract

The innate immune response comprises the initial events that occur during tissue insult, causing cellular activation and triggering inflammation. Innate immune cells, including resident and early migrated cells from the bloodstream, sense a plethora of molecules called molecular patterns, that are derived from microorganisms or host cells. Once activated, pattern recognition receptor (PRR) signalling is triggered intracellularly and promotes the synthesis and release of vasoactive molecules, which target endothelial cells and cause inflammation. In addition, circulating molecules and pathogens also activate PRRs that are expressed on endothelial cells. These events modify endothelial cell metabolism, changing their conformational state and promoting the expression of pro-inflammatory molecules. Importantly, gain-of-function mutations in PRRs are associated with continuous cellular activation, leading to the development of autoinflammatory diseases. Here, we discuss the relationship among the cellular and humoral arms of the innate immune system in inflammatory processes, with special attention given to endothelial cell activation.