Journal Article

PUBDB-2024-05768

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Kupffer cell–like syncytia replenish resident macrophage function in the fibrotic liver

Peiseler, M. ; Araujo David, B. ; Zindel, J. ; Surewaard, B. G. J. ; Lee, W.-Y. ; Heymann, F. ; Nusse, Y. ; Castanheira, F. V. S. ; Shim, R. ; Guillot, A. ; Bruneau, A. ; Atif, J. ; Perciani, C. ; Ohland, C. ; Ganguli Mukherjee, P. ; Niehrs, A. ; Thünauer, R.Extern*CSSB* ; Altfeld, M. ; Amrein, M. ; Liu, Z. ; Gordon, P. M. K. ; McCoy, K. ; Deniset, J. ; MacParland, S. ; Ginhoux, F. ; Tacke, F. ; Kubes, P. (Corresponding author)

2023
Assoc. Washington, DC

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Please use a persistent id in citations: doi:10.1126/science.abq5202

Abstract: Kupffer cells (KCs) are specialized macrophages in the liver sinusoids that filter bacteria in the bloodstream. Liver fibrosis and cirrhosis, a common pathology of chronic liver disease, leads to the redistribution of blood flow from the sinusoids to collateral vessels. Using a mouse model of hepatic fibrosis, Peiseler et al. report that remodeling of the liver causes KCs to lose contact with surrounding cells and lose their distinct cellular identity (see the Perspective by Louwe and Guilliams). The liver still maintains its bacterial filtration function because the presence of a microbiome helps to recruit monocytes to large intrahepatic vessels, where they fuse into large cell aggregates that exhibit a KC-like phenotype. These KC-like syncytia show enhanced bacterial capture capacity and are present in cirrhotic livers from patients with various chronic liver diseases. —Seth Thomas Scanlon

Note: Deutsche Forschungsgemeinschaft: PE2737/1-1Deutsche Forschungsgemeinschaft: PE2737/1-1

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Contributing Institute(s):

1. CSSB-CF-ALFM (CSSB-CF-ALFM)

Research Program(s):

1. 899 - ohne Topic (POF4-899) (POF4-899)

Experiment(s):

1. No specific instrument

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