scholarly journals Contributory Role of BLT2 in the Production of Proinflammatory Cytokines in Cecal Ligation and Puncture-Induced Sepsis

2021 ◽  
Author(s):  
Donghwan Park ◽  
MyungJa Ro ◽  
A-Jin Lee ◽  
Dong-Wook Kwak ◽  
Yunro Chung ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture

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 Role of Lipopolysaccharide and Cecal Ligation and Puncture on Blood Coagulation and Inflammation in Sensitive and Resistant Mice Models

2005 ◽  
Vol 166 (4) ◽  
pp. 1089-1098 ◽  
Author(s):  
Javier Corral ◽  
José Yélamos ◽  
David Hernández-Espinosa ◽  
Yolanda Monreal ◽  
Ruben Mota ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture

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.

scholarly journals Kinetics and protective role of autophagy in a mouse cecal ligation and puncture-induced sepsis

Critical Care ◽  
2013 ◽  
Vol 17 (4) ◽  
pp. R160 ◽  
Author(s):  
Waka Takahashi ◽  
Eizo Watanabe ◽  
Lisa Fujimura ◽  
Haruko Watanabe-Takano ◽  
Hiroyuki Yoshidome ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
Protective Role ◽  
Cecal Ligation And Puncture

ROLE OF INTERFERON-GAMMA IN LUNG INFLAMMATION FOLLOWING CECAL LIGATION AND PUNCTURE IN RATS

Shock ◽  
1999 ◽  
Vol 12 (3) ◽  
pp. 215-221 ◽  
Author(s):  
Kingsley Yin ◽  
Carl E. Hock ◽  
Pi-Shiang Lai ◽  
Jason T. Ross ◽  
Gang Yue
Keyword(s):  
Interferon Gamma ◽  
Lung Inflammation ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture

scholarly journals Intestinal permeability is reduced and IL-10 levels are increased in septic IL-6 knockout mice

2001 ◽  
Vol 281 (3) ◽  
pp. R1013-R1023 ◽  
Author(s):  
Quan Wang ◽  
Cheng Hui Fang ◽  
Per-Olof Hasselgren
Keyword(s):  
Intestinal Permeability ◽  
Cecal Ligation ◽  
Fluorescein Isothiocyanate ◽  
Sham Operation ◽  
Cecal Ligation And Puncture ◽  
Wild Type ◽  
Mucosal Permeability ◽  
Ussing Chambers ◽  
Intestinal Segments

Sepsis is associated with increased intestinal permeability, but mediators and mechanisms are not fully understood. We examined the role of interleukin (IL)-6 and IL-10 in sepsis-induced increase in intestinal permeability. Intestinal permeability was measured in IL-6 knockout (IL-6 −/−) and wild-type (IL-6 +/+) mice 16 h after induction of sepsis by cecal ligation and puncture or sham operation. In other experiments, mice or intestinal segments incubated in Ussing chambers were treated with IL-6 or IL-10. Intestinal permeability was assessed by determining the transmucosal transport of the 4.4-kDa marker fluorescein isothiocyanate conjugated dextran and the 40-kDa horseradish peroxidase. Intestinal permeability for both markers was increased in septic IL-6 +/+ mice but not in septic IL-6 −/− mice. Treatment of nonseptic mice or of intestinal segments in Ussing chambers with IL-6 did not influence intestinal permeability. Plasma IL-10 levels were increased in septic IL-6 −/− mice, and treatment of septic mice with IL-10 resulted in reduced intestinal permeability. Increased intestinal permeability during sepsis may be regulated by an interaction between IL-6 and IL-10. Treatment with IL-10 may prevent the increase in mucosal permeability during sepsis.

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