Sepsis is a dysfunctional systemic inflammatory response to bacterial infection in the body. White blood cell recruitment is a hallmark of sepsis and is associated with endothelial cells (EC). EC are blood vessel wall cells in direct contact with blood and can be activated by lipopolysaccharide, a bacterial component. In activated EC, transcription factors (TF) are activated and move to the nucleus, regulating the expression of genes encoding, among others, adhesion molecules. White blood cells interact with adhesion molecules, facilitating their recruitment and transendothelial migration into the tissue, which protects the body against invading microorganisms. Yet molecular mechanisms of activated EC in the recruitment of white blood cells in sepsis have not been completely elucidated.
The overarching aim of this thesis of Zhendong Wang was to investigate the activation status of EC responding to harmful stimuli in the kidney, lung, and liver during sepsis. Exploration of endothelial activation contributes to understanding its roles in the recruitment of white blood cells in these three organs and is necessary before future therapeutic design.
I explored the spatiotemporal pattern of activation of inflammation-associated TF, expression of adhesion molecules, and recruitment of white blood cell subsets in these three organs in septic mice.
I mainly found that in the early stages of sepsis, the recruitment of white blood cell subsets, expression of adhesion molecules, and activation of TF studied are likely organ-specific.
Future studies should further explore the relationship between endothelial activation and recruitment of white blood cells in septic mice by deleting endothelial-related TF.
