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Correction

Correction: The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis

  • PLOS Pathogens Staff

Fig 3 is incorrect. The authors have provided a corrected version here. The publisher apologizes for the error.

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Fig 3. MHV-3 fails to induce FGL2 production and neutrophil infiltration in the livers of IL-1R1-/- mice.

IL-1R1-/- mice and their C57BL/6 WT littermates were infected with MHV-3 (100 PFU). (A) Peritoneal exudative macrophages (PEMs) were isolated and the expression of FGL2 was detected by western-blotting. (B) The expression of FGL2 in liver at 48h and 72h post-infection was analyzed by western-blotting. Four representative samples per group are shown. (C) Serum FGL2 levels in virus infected mice were measured by ELISA.*p<0.05 and **p<0.0001, NS: no significant difference, n = 5 per group. (D) The liver fibrinogen deposition post-infection was analyzed by immunohistochemistry. Scale bar 20 μm, n = 6~8 per group. (E) Liver recruitment of CD45+Gr-1high neutrophils after MHV-3 infection was measured by flow cytometry. The left panels are gate strategies, and number indicates the percentage of positive cells in the gate. One representative sample from five mice per group is showed. (F) Statistical analysis of liver CD45+Gr-1high neutrophil infiltration. *p<0.05 compared to WT littermates in each group, n = 5 per group.

https://doi.org/10.1371/journal.ppat.1005406.g001

Reference

  1. 1. Guo S, Yang C, Diao B, Huang X, Jin M, Chen L, et al. (2015) The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis. PLoS Pathog 11(9): e1005155. pmid:26367131

Citation: PLOS Pathogens Staff (2016) Correction: The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis. PLoS Pathog 12(2): e1005406. https://doi.org/10.1371/journal.ppat.1005406

Published: February 29, 2016

Copyright: © 2016 PLOS Pathogens Staff. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.