Regulation of the Inflammatory Process by SECs

Exposure of the SECs to pathogens or cytokines produced by other cells during stress induces activation of the SECs and subsequent production of cytokines, eicosanoids, and/or adhesion molecules. For instance, after activation with EPS, a main component of the walls of gramnegative bacteria and a major inducer of inflammation and non-specific immune functions [20], SECs produce a number of pro- and anti-inflammatory cytokines. Pro-inflammatory cytokines shown to be produced were tumour necrosis factor alpha (TNFa) [26] interleukin-1 alpha/beta(IL-lo/p) [27] the major inducer of acute phase proteins interleukin-6 (IL-6) [28] and the neutrophil chemo-attractant interleukin-8 (IL-8) [29]. Anti-inflammatory cytokines shown to be produced were interleukin-10 (IL-10) [27] and hepatocyte growth factor (HGF) [30]. 

like the vascular endothehum, play an active part in the control of leucocyte recruitment in cases of acute and chronic inflammatory conditions. Eeucocyte recruitment from the blood compartment is a crucial determinant for the induction of immunity and inflammation. SECs control this process by producing cytokines that activate leucocytes and by expressing adhesion molecules. Under inflammatory conditions upregulation of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was found [35 36], as well as expression of E-selectin and P-selectin [37]. Together with the expression of CD4 on SECs it has been postulated that these adhesion molecules might also be involved in the adhesion of KC cells to the sinusoidal wall [20]. 

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