scholarly journals PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Weimin Zhu ◽  
Rui Bao ◽  
Xiaohua Fan ◽  
Tianzhu Tao ◽  
Jiali Zhu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Phase Proteins ◽  
Therapeutic Potential ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture ◽  
Host Immune Responses ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Puncture Model

Liver plays a major role in hypermetabolism and produces acute phase proteins during systemic inflammatory response syndrome and it is of vital importance in host defense and bacteria clearance. Our previous studies indicated that programmed death-1 (PD-1) and its ligand programmed death ligand-1 (PD-L1) are crucial modulators of host immune responses during sepsis. Our current study was designed to investigate the role of PD-L1 in sepsis-induced liver injury by a mouse cecal ligation and puncture (CLP) model. Our results indicated that there was a significant increase of PD-L1 expression in liver after CLP challenge compared to sham-operated controls, in terms of levels of mRNA transcription and immunohistochemistry. Anti-PD-L1 antibody significantly alleviated the morphology of liver injury in CLP mice. Anti-PD-L1 antibody administration decreased ALT and AST release in CLP mice, decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 mRNA in liver after sepsis challenge. Thus, anti-PD-L1 antibody might have a therapeutic potential in attenuating liver injury in sepsis.

Induction of the NEK family of kinases in the lungs of mice subjected to cecal ligation and puncture model of sepsis

2021 ◽  
pp. 1929787
Author(s):  
Mohammad A. Uddin ◽  
Mohammad S. Akhter ◽  
Khadeja-Tul Kubra ◽  
Nektarios Barabutis
Keyword(s):  
Cecal Ligation ◽  
Cecal Ligation And Puncture ◽  
Puncture Model

scholarly journals Hypertonic Saline Solution Drives Neutrophil from Bystander Organ to Infectious Site in Polymicrobial Sepsis: A Cecal Ligation and Puncture Model

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74369 ◽  
Author(s):  
Mariana Cardillo Theobaldo ◽  
Flavia Llimona ◽  
Ricardo Costa Petroni ◽  
Ester Correia Sarmento Rios ◽  
Irineu Tadeu Velasco ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Saline Solution ◽  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Cecal Ligation And Puncture ◽  
Hypertonic Saline Solution ◽  
Puncture Model

scholarly journals Protective Role of Programmed Death 1 Ligand 1 (PD-L1)in Nonobese Diabetic Mice: The Paradox in Transgenic Models

Diabetes ◽  
2008 ◽  
Vol 57 (7) ◽  
pp. 1861-1869 ◽  
Author(s):  
C.-J. Wang ◽  
F.-C. Chou ◽  
C.-H. Chu ◽  
J.-C. Wu ◽  
S.-H. Lin ◽  
...  
Keyword(s):  
Protective Role ◽  
Diabetic Mice ◽  
Transgenic Models ◽  
Nonobese Diabetic ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Nonobese Diabetic Mice

scholarly journals Protective Role of Coenzyme Q10 in Acute Sepsis-Induced Liver Injury in BALB/c Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Qian-wei Li ◽  
Qin Yang ◽  
Hong-Yang Liu ◽  
Yu-ling Wu ◽  
Yu-Hua Hao ◽  
...  
Keyword(s):  
Liver Injury ◽  
Coenzyme Q10 ◽  
Cecal Ligation ◽  
Protective Role ◽  
Hepatic Tissue ◽  
Control Group ◽  
Cecal Ligation And Puncture ◽  
Sequestosome 1

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1β, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-α expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.

scholarly journals A study for a role of inducible NO synthase in septic rats with cecal ligation and puncture (CLP)

1999 ◽  
Vol 79 ◽  
pp. 97
Author(s):  
Masayoshi Abe ◽  
Iku Okamoto ◽  
Kazuhiko Shibata ◽  
Keiichi Tanaka ◽  
Noriyuki Sakata ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
No Synthase ◽  
Cecal Ligation And Puncture ◽  
Inducible No Synthase

scholarly journals Necrostatin-1 accelerates time to death in a rat model of cecal ligation and puncture and massively increases hepatocyte caspase-3 cleavage

2019 ◽  
Vol 316 (4) ◽  
pp. G551-G561 ◽  
Author(s):  
Qin Zhang ◽  
Siwei Wei ◽  
Jiayin Lu ◽  
Weijun Fu ◽  
Hui Chen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Liver Injury ◽  
Survival Time ◽  
Caspase 3 ◽  
Cecal Ligation ◽  
B Cell Lymphoma ◽  
Cecal Ligation And Puncture ◽  
Interacting Protein ◽  
Regulated Necrosis ◽  
Related Proteins

Necroptosis, a form of regulated necrosis, has been reported to be involved in numerous pathologies, including sepsis. However, a protective effect of the selective inhibitor of necroptosis, necrostatin-1 (Nec-1), against sepsis remains to be confirmed. Animals (rats and mice) were subjected to cecal ligation and puncture (CLP) to mimic clinical sepsis. Nec-1 or its vehicle (control) was administered 20 min before CLP. Survival time was observed up to 72 h after CLP. Specimens of liver tissue and serum were obtained at 6 h, 12 h, and 18 h. Expression of necroptosis-related proteins [receptor-interacting protein kinase (RIP)1, RIP3, and mixed lineage kinase domain-like (MLKL)] was determined by Western blot analysis. The RIP1/RIP3 interaction and the recruitment of MLKL to RIP3 were also analyzed. Liver function, histopathological changes, serum inflammation cytokines, TUNEL staining, and the expression of apoptosis-related protein, including caspase-3, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X (Bax), was determined. As expected, Nec-1 administration reduced the expression of necroptosis-related proteins and the RIP1/RIP3 interaction, indicating inhibited necroptosis. Surprisingly, Nec-1 treatment exacerbated the liver injury and shortened survival time of septic rats with increased TUNEL-positive cells, cleaved caspase-3 protein content, and Bax/Bcl-2 ratio. Collectively, these findings show that Nec-1 administration inhibited the hepatocyte necroptosis pathway but accelerated apoptosis via the apoptotic pathway in CLP-induced sepsis rat. NEW & NOTEWORTHY The present study demonstrated that a chemical inhibitor necrostatin-1 (Nec-1) or receptor-interacting protein kinase(RIP1) knock down targeted at necroptosis inhibition accelerated liver injury of following sepsis. For fundamental research, these results warrant further investigation of the potential link between Nec-1 administration and the cellular apoptosis following sepsis induced liver injury. For applied research, these results suggest the potential harmful effect of Nec-1 on future sepsis treatment.

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