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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Gut. 2009 May;58(5):704–720. doi: 10.1136/gut.2008.156307

Figure 4. Promotion of hepatic stellate cell activation and fibrosis by LPS.

Figure 4

Following liver injury, alterations in the bacterial microbiota and the intestinal mucosal barrier cause an increase in the translocation of LPS. LPS directly targets quiescent hepatic stellate cells resulting in (i) downregulation of the TGFβ pseudoreceptor Bambi and (ii) upregulation of chemokines. These two signals complement each other to promote hepatic stellate cell activation: 1. Downregulation of Bambi through a TLR4-MyD88-NF-κB signaling cascade sensitizes hepatic stellate cells towards the effect of TGFβ. 2. Chemokines induce Kupffer cells, a main source of TGFβ in the injured liver, to migrate towards hepatic stellate cells. Together, these two mechanisms allow TGFβ-dependent activation of hepatic stellate cell by Kupffer cells resulting in increased deposition of extracellular matrix and liver fibrosis.