Background: Adhesion of polymorphonuclear leukocytes (PMN) to endothelial cells and subsequent transendothelial migration are an early key events in the inflammatory response and play an important part in the pathogenesis of septic shock, contributing to vascular and tissue injury. Taurine (2-aminoethanesulfonic acid) is a sulphur-containing beta amino acid. It is a known antioxidant, possesses antimicrobial properties, and has previously been shown to be protective to the endothelium both in vivo and in vitro. The aim of this study was to determine if pretreatment with taurinewould attenuate the lipopolysaccharide (LPS)-induced increase in leukocyte-endothelial interactions and microvascular permeability during endotoxemia.

Materials and methods: Male Sprague-Dawley rats (300-350 g) were randomized into three groups: (1) Control, (2) LPS, and (3) LPS + Taurine groups. Taurine was administered orally as a 4% solution. Endotoxemia was induced using Escherichia Coli endotoxin (Serotype 0.55 B5)-15 mg/kg via a slow intravenous infusion. Using mesenteric postcapillary venules (28-32-microm diameter) the number of adherent and migrated leukocytes and their rolling velocity were measured by intravital microscopy at baseline and subsequently at 10, 30, 60, and 90 min post administration of LPS.

Results: Following administration of LPS there was a reduction in leukocyte rolling velocity at 30, 60 and 90 min. This was accompanied by a significant increase in the number of adherent leukocytes at 10, 30, 60 and 90 min. Transendothelial migration was significantly increased at 90 min. Taurine significantly attenuated the LPS-induced reduction in leukocyte rolling velocity at 10 and 30 min and the number of adherent leukocytes at all time points. Taurine also attenuated the LPS-induced increase in transendothelial migration at 90 min.

Conclusions: These results demonstrate that taurine ameliorates endotoxin-induced leukocyte-endothelial cell interactions associated with sepsis, thereby suggesting that taurine may have a therapeutic role in the preventionof endothelial damage in sepsis.