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. 2021 Oct 1;10(10):2618. doi: 10.3390/cells10102618

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Nlrp3^−/− ameliorated severe liver damage and proinflammatory milieu after LCA feeding. Nlrp3^−/− attenuated severe liver damage after LCA feeding with smaller necrotic areas, fewer bile infarcts and lowered transaminase levels (A,E). However, normal morphology was not obtained. Nlrp3^−/− mice revealed lower Caspase-1 activity and Il-1b mRNA levels (B,F). Despite NLRP3 deficiency fibrotic markers remained the same (D,H), whereas infiltration of inflammatory, MPO-positive cells decreased (C). Nlrp3^−/− inhibited a proinflammatory environment after LCA feeding as indicated by decreased mRNA markers of immune cell invasion (F4/80, Cd68, Mcp1) and proinflammatory macrophages (Tnf, iNos, Il-18) (G). * p < 0.05; ** p < 0.01; *** p < 0.001; n.d.: not detected; n = 6.