Sepsis is an archetypal condition with molecular links between inflammation and coagulation. Both events can be orchestrated by the interaction between circulating and vascular cells that under activation release microparticles. Recently, we reported that increased circulating microparticles in septic patients play a pivotal role in ex vivo vascular function suggesting that they are protective against vascular hyporeactivity by maintaining a tonic pressor response (Mostefai et al. Am J Resp Crit Care Med 2008). Besides, we further demonstrated these effects of septic microparticles in human tissue-engineered blood vessel models by comparing the contractile response to histamine of two vascular constructs from human vascular smooth muscle cells and fibroblasts. The first model is composed of a media solely (TEVM), and the second contained a media and an adventitia (TEVMA). Indeed, we showed that septic microparticles increased contraction induced by histamine, in vascular constructs from TEVM but not in TEVMA. This effect was linked to their capacity to decrease vasodilators components, from inducible nitric oxide synthase and cyclooxygenase-2 (COX-2), and increase mRNA expression of IL-10 in TEVM The present study was designed to address the question whether IL-10 is the mediator implicated in the protective effect of septic microparticles against vascular hyporeactivity observed in sepsis using the two vascular constructs, TEVM and TEVMA. For this purpose, the effect of IL-10 was investigated in the two constructs in presence or absence of lipopolysaccharide (LPS). IL-10 treatment did not modify the contractile response in both TEVM and TEVMA compared to non-treated vessels. LPS treatment induced vascular hyporeactivity in TEVM but it did not modify the contractile response in TEVMA compared to non-treated vessels. Interestingly, IL-10 restores contraction in LPS-treated TEVM towards control vessels. The mechanisms by which IL-10 enhanced the response are under investigation in relation with the COX vasoconstrictor metabolite, thromboxane A2, as reported in our previous manuscript (Mostefai et al. 2008). These data demonstrate that IL-10 restores the vascular hyporeactivity induced by LPS in tissue-engineered blood vessel models.