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2016-10-18

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cc-by (c) Odena, Gemma et al., 2016
Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/112427

LPS-TLR4 Pathway mediates ductular cell expansion in alcoholic hepatitis.

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https://doi.org/10.1038/srep35610

Abstract

Alcoholic hepatitis (AH) is the most severe form of alcoholic liver disease for which there are no effective therapies. Patients with AH show impaired hepatocyte proliferation, expansion of inefficient ductular cells and high lipopolysaccharide (LPS) levels. It is unknown whether LPS mediates ductular cell expansion. We performed transcriptome studies and identified keratin 23 (KRT23) as a new ductular cell marker. KRT23 expression correlated with mortality and LPS serum levels. LPS-TLR4 pathway role in ductular cell expansion was assessed in human and mouse progenitor cells, liver slices and liver injured TLR4 KO mice. In AH patients, ductular cell expansion correlated with portal hypertension and collagen expression. Functional studies in ductular cells showed that KRT23 regulates collagen expression. These results support a role for LPS-TLR4 pathway in promoting ductular reaction in AH. Maneuvers aimed at decreasing LPS serum levels in AH patients could have beneficial effects by preventing ductular reaction development.

Subject

Hepatitis, Alcoholisme, Proliferació cel·lular

Subject (English)

Hepatitis, Alcoholism, Cell proliferation

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Articles publicats en revistes (Medicina)
Articles publicats en revistes (IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer)

Citation

ODENA, Gemma, et al. LPS-TLR4 Pathway mediates ductular cell expansion in alcoholic hepatitis. Scientific Reports. 2016. Vol. 6, num. 35610. ISSN 2045-2322. [consulted: 17 of August of 2026]. Available at: https://hdl.handle.net/2445/112427

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