Gut-liver axis in liver cirrhosis: How to manage leaky gut and endotoxemia

Figure 1 Mechanism of lipopolysaccharide clearance in the blood and LPS-toll like receptors-MyD88 signal transduction. LBP enhances cell responses to LPS by accelerating the binding of LPS to CD14. LBP can also inhibit cell responses to LPS; It transfers LPS to plasma lipoproteins and it combines with LPS aggregates to form large LPS-LBP complexes that are internalized[176]. sCD14 can remove, or divert, LPS from mCD14 and transfer it to plasma lipoproteins, where LPS is inactivated[176]. Albumin is essential during the interaction of LBP with LPS aggregate to produce a LBP: LPS aggregate and the efficient transfer of LPS from the aggregate to a molecule of sCD14[177]. Albumin stabilizes LPS: CD14 complexes for cell activation. Mechanism of inhibitory effect of albumin on LPS is still unknown. It may directly inactivate minute amount of LPS and may also enhance LPS transport to lipoproteins. LPS: Lipopolysaccharide; LBP: Lipopolysaccharide binding protein; TNF-α: Tumor necrosis factor α; TLR4: Toll-like receptors 4; NF-κB: Nuclear factor kappa B; TRAF6: TNF receptor-associated factor.