scholarly journals Bone marrow-derived macrophages distinct from tissue-resident macrophages play a pivotal role in Concanavalin A-induced murine liver injury via CCR9 axis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Takeru Amiya ◽  
Nobuhiro Nakamoto ◽  
Po-sung Chu ◽  
Toshiaki Teratani ◽  
Hideaki Nakajima ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Concanavalin A ◽  
Pivotal Role ◽  
Murine Liver

scholarly journals Macrophage inflammatory protein-2 induced by TNF-α plays a pivotal role in concanavalin A-induced liver injury in mice

2001 ◽  
Vol 35 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Kimihide Nakamura ◽  
Mitsuyoshi Okada ◽  
Masashi Yoneda ◽  
Shujiro Takamoto ◽  
Yukiomi Nakade ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A ◽  
Pivotal Role ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Macrophage Inflammatory Protein

scholarly journals PARP2 deficiency affects invariant-NKT-cell maturation and protects mice from concanavalin A-induced liver injury

2017 ◽  
Vol 313 (5) ◽  
pp. G399-G409 ◽  
Author(s):  
Aveline Filliol ◽  
Claire Piquet-Pellorce ◽  
Sarah Dion ◽  
Valentine Genet ◽  
Catherine Lucas-Clerc ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Concanavalin A ◽  
Immune Cell ◽  
Cell Populations ◽  
Genetic Inactivation ◽  
Hepatocyte Death ◽  
Invariant Natural Killer ◽  
Deficient Mice ◽  
Nkt Lymphocytes

Excessive or persistent inflammation and hepatocyte death are the key triggers of liver diseases. The poly(ADP-ribose) polymerase (PARP) proteins induce cell death and inflammation. Chemical inhibition of PARP activity protects against liver injury during concanavalin A (ConA)-induced hepatitis. In this mice model, ConA activates immune cells, which promote inflammation and induce hepatocyte death, mediated by the activated invariant natural killer T (iNKT) lymphocyte population. We analyzed immune cell populations in the liver and several lymphoid organs, such as the spleen, thymus, and bone marrow in Parp2-deficient mice to better define the role of PARP proteins in liver immunity and inflammation at steady state and during ConA-induced hepatitis. We show that 1) the genetic inactivation of Parp2, but not Parp1, protected mice from ConA hepatitis without deregulating cytokine expression and leucocyte recruitment; 2) cellularity was lower in the thymus, but not in spleen, liver, or bone marrow of Parp2−/− mice; 3) spleen and liver iNKT lymphocytes, as well as thymic T and NKT lymphocytes were reduced in Parp2 knockout mice. In conclusion, our results suggest that the defect of T-lymphocyte maturation in Parp2 knockout mice leads to a systemic reduction of iNKT cells, reducing hepatocyte death during ConA-mediated liver damage, thus protecting the mice from hepatitis. NEW & NOTEWORTHY The genetic inactivation of Parp2, but not Parp1, protects mice from concanavalin A hepatitis. Immune cell populations are lower in the thymus, but not in the spleen, liver, or bone marrow of Parp2-deficient mice compared with wild-type mice. Spleen and liver invariant natural killer T (NKT) lymphocytes, as well as thymic T and NKT lymphocytes, are reduced in Parp2-deficient mice.

The role of microbiota in concanavalin A-mediated liver injury

2018 ◽  
Vol 56 (01) ◽  
pp. E2-E89
Author(s):  
B Schiller ◽  
C Wegscheid ◽  
L Berkhout ◽  
A Zarzycka ◽  
U Steinhoff ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A

scholarly journals Liver Injury and the Macrophage Issue: Molecular and Mechanistic Facts and Their Clinical Relevance

2021 ◽  
Vol 22 (14) ◽  
pp. 7249
Author(s):  
Siyer Roohani ◽  
Frank Tacke
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Current Knowledge ◽  
Hepatocellular Cancer ◽  
Complete Recovery ◽  
Hepatic Macrophages ◽  
Liver Injuries ◽  
Microbial Products ◽  
Injured Liver

The liver is an essential immunological organ due to its gatekeeper position to bypassing antigens from the intestinal blood flow and microbial products from the intestinal commensals. The tissue-resident liver macrophages, termed Kupffer cells, represent key phagocytes that closely interact with local parenchymal, interstitial and other immunological cells in the liver to maintain homeostasis and tolerance against harmless antigens. Upon liver injury, the pool of hepatic macrophages expands dramatically by infiltrating bone marrow-/monocyte-derived macrophages. The interplay of the injured microenvironment and altered macrophage pool skews the subsequent course of liver injuries. It may range from complete recovery to chronic inflammation, fibrosis, cirrhosis and eventually hepatocellular cancer. This review summarizes current knowledge on the classification and role of hepatic macrophages in the healthy and injured liver.

Dregea volubilisAmeliorates Concanavalin A-Induced Liver Injury by Facilitating Apoptosis of Activated T Cells

2008 ◽  
Vol 233 (9) ◽  
pp. 1124-1132 ◽  
Author(s):  
Fangyuan Gong ◽  
Yan Shen ◽  
Chaofeng Zhang ◽  
Jianliang Xu ◽  
Xuefeng Wu ◽  
...  
Keyword(s):  
T Cells ◽  
Liver Injury ◽  
Concanavalin A ◽  
Activated T Cells

Dietary phosphatidylinositol protects C57BL/6 mice from concanavalin A-induced liver injury by modulating immune cell functions

2013 ◽  
Vol 57 (9) ◽  
pp. 1671-1679 ◽  
Author(s):  
Masashi Inafuku ◽  
Koji Nagao ◽  
Ayako Inafuku ◽  
Teruyoshi Yanagita ◽  
Naoyuki Taira ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A ◽  
Immune Cell ◽  
Cell Functions

scholarly journals Fucosterol Protects against Concanavalin A-Induced Acute Liver Injury: Focus on P38 MAPK/NF-κB Pathway Activity

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Wenhui Mo ◽  
Chengfen Wang ◽  
Jingjing Li ◽  
Kan Chen ◽  
Yujing Xia ◽  
...  
Keyword(s):  
Liver Injury ◽  
P38 Mapk ◽  
Concanavalin A ◽  
Molecular Mechanisms ◽  
Therapeutic Agent ◽  
Acute Liver Injury ◽  
Biological Activities ◽  
Hepatic Necrosis ◽  
Protective Effects ◽  
Eisenia Bicyclis

Objective. Fucosterol is derived from the brown alga Eisenia bicyclis and has various biological activities, including antioxidant, anticancer, and antidiabetic properties. The aim of this study was to investigate the protective effects of fucosterol pretreatment on Concanavalin A- (ConA-) induced acute liver injury in mice, and to understand its molecular mechanisms. Materials and Methods. Acute liver injury was induced in BALB/c mice by ConA (25 mg/kg), and fucosterol (dissolved in 2% DMSO) was orally administered daily at doses of 25, 50, and 100 mg/kg. The levels of hepatic necrosis, apoptosis, and autophagy associated with inflammatory cytokines were measured at 2, 8, and 24 h. Results. Fucosterol attenuated serum liver enzyme levels and hepatic necrosis and apoptosis induced by TNF-α, IL-6, and IL-1β. Fucosterol also inhibited apoptosis and autophagy by upregulating Bcl-2, which decreased levels of functional Bax and Beclin-1. Furthermore, reduced P38 MAPK and NF-κB signaling were accompanied by PPARγ activation. Conclusion. This study showed that fucosterol could alleviate acute liver injury induced by ConA by inhibiting P38 MAPK/PPARγ/NF-κB signaling. These findings highlight that fucosterol is a promising potential therapeutic agent for acute liver injury.

scholarly journals Pivotal role of nuclear factor ?B signaling in anti-CD40-induced liver injury in mice

Hepatology ◽  
2004 ◽  
Vol 40 (5) ◽  
pp. 1180-1189 ◽  
Author(s):  
Kiminori Kimura ◽  
Masahito Nagaki ◽  
Shinji Takai ◽  
Shinichi Satake ◽  
Hisataka Moriwaki
Keyword(s):  
Liver Injury ◽  
Pivotal Role ◽  
Nuclear Factor ◽  
Factor B
Sign in / Sign up

Export Citation Format

Share Document