scholarly journals CO2Pneumoperitoneum Preservesβ-Arrestin 2 Content and Reduces High Mobility Group Box-1 (HMGB-1) Expression in an Animal Model of Peritonitis

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Angela Simona Montalto ◽  
Alessandra Bitto ◽  
Letteria Minutoli ◽  
Pietro Impellizzeri ◽  
Gaetano Costa ◽  
...  
Keyword(s):  
Bacterial Load ◽  
Cecal Ligation ◽  
Signal Transduction Pathway ◽  
High Mobility ◽  
Receptor Activation ◽  
High Mobility Group ◽  
Male Rats ◽  
Toll Like Receptor ◽  
To Receive ◽  
Lung And Kidney

Laparoscopy (LS) has been shown to decrease the inflammatory sequelae of endotoxemia.β-arrestin 2 plays an important function in signal transduction pathway of TLR4. High mobility group box-1 (HMGB-1) is involved in the delayed systemic inflammatory response. We investigated the effects of CO2insufflation on liver, lung, and kidney expression of bothβ-arrestin 2 and HMGB-1 during sepsis. Cecal ligation and puncture (CLP) was performed in male rats and 6 h later the animals were randomly assigned to receive a CO2pneumoperitoneum or laparotomy. Animals were euthanized; liver, lung, and kidney were removed for the evaluation ofβ-arrestin 2 and HMGB-1 expression. Immunohistochemical detection of myeloperoxidase (MPO) was investigated in lung and liver and bacterial load was determined in the peritoneal fluid. CO2pneumoperitoneum reduced peritoneal bacterial load, increased the expression ofβ-arrestin 2, and blunted the expression of the potent proinflammatory HMGB-1 in liver, lung, and kidney compared with laparotomy. Liver and lung MPO was markedly reduced in rats subjected to LS compared with laparotomy. We believe that CO2exerts an early protective effect by reducing bacterial load and likely toll-like receptor activation which in turn leads to a preservedβ-arrestin 2 expression and a reduced HMGB-1 expression.

Glucocorticoid Modulates High-Mobility Group Box 1 Expression and Toll-Like Receptor Activation in Obstructive Jaundice

2011 ◽  
Vol 170 (1) ◽  
pp. e47-e55 ◽  
Author(s):  
Ying-Hsien Huang ◽  
Pei-Wen Wang ◽  
Mao-Meng Tiao ◽  
Ming-Huei Chou ◽  
Yung-Ying Du ◽  
...  
Keyword(s):  
Obstructive Jaundice ◽  
High Mobility ◽  
Receptor Activation ◽  
High Mobility Group ◽  
Toll Like Receptor

scholarly journals The effects of n-3 PUFA and intestinal lymph drainage on high-mobility group box 1 and Toll-like receptor 4 mRNA in rats with intestinal ischaemia–reperfusion injury

2011 ◽  
Vol 108 (5) ◽  
pp. 883-892 ◽  
Author(s):  
Gui-Zhen He ◽  
Kai-Guo Zhou ◽  
Rui Zhang ◽  
Xue-Feng Chen
Keyword(s):  
Inflammatory Cytokine ◽  
High Mobility ◽  
High Mobility Group ◽  
Male Rats ◽  
Intestinal Ischaemia ◽  
Toll Like Receptor ◽  
Lymph Drainage ◽  
Intestinal Lymph ◽  
Ischaemia Reperfusion ◽  
Tlr4 Mrna

The aim of the present study was to investigate the impacts of n-3 PUFA and lymph drainage (D) on intestinal ischaemia–reperfusion (I/R) injury in rats. A total of forty-eight Sprague–Dawley male rats were randomly divided into three groups (n 16): normal diet (N), enteral nutrition (EN) and EN plus n-3 PUFA. Each group was further divided into lymph drainage (I/R+D) and non-drainage (I/R) sub-groups (n 8). After 5 d with different nutrition regimens, the rats were subjected to 60 min ischaemia by clamping the superior mesenteric artery, followed by 120 min reperfusion. At the same time, the rats in the I/R+D sub-groups were treated with intestinal lymph drainage for 180 min. Organs were harvested and we detected the cytokine, endotoxin, and expression of Toll-like receptor (TLR) 4 mRNA and its endogenous ligand high-mobility group box 1 (HMGB1). We found that the serum levels of HMGB1, inflammatory cytokine and endotoxin in the three I/R+D sub-groups were significantly lower than those in the N (I/R) and EN (I/R) sub-groups (P < 0·05). The activation of NF-κB and the expression of HMGB1 and TLR4 mRNA significantly increased in the jejunum, ileum, liver and lung after intestinal I/R injury, but notably lower in the I/R+D groups than those in I/R (P < 0·05). The injury degree and HMGB1 expression were decreased in the n-3 PUFA group than in the N and EN groups. We preliminarily concluded that nutrition with n-3 PUFA and/or intestinal lymph drainage may reduce HMGB1 and inflammatory cytokine in serum and lymph and inhibit the expression and signal transmission of TLR4 mRNA, thereby alleviating intestinal I/R injury in rats.

scholarly journals TNF-α Activates High-Mobility Group Box 1 - Toll-Like Receptor 4 Signaling Pathway in Human Aortic Endothelial Cells

2016 ◽  
Vol 38 (6) ◽  
pp. 2139-2151 ◽  
Author(s):  
Won Seok Yang ◽  
Nam Jeong Han ◽  
Jin Ju Kim ◽  
Mee Jeong Lee ◽  
Su-Kil Park
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
High Mobility ◽  
Neutralizing Antibody ◽  
High Mobility Group ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Aortic Endothelial Cells ◽  
Tnf Α ◽  
Human Aortic Endothelial Cells

Background/Aims: Toll-like receptor 4 (TLR4) interacts with endogenous substances as well as lipopolysaccharide. We explored whether TLR4 is implicated in tumor necrosis factor-α (TNF-α) signal transduction in human aortic endothelial cells. Methods: The pathway was evaluated by transfection of siRNAs, immunoprecipitation and Western blot analysis. Results: TNF-α activated spleen tyrosine kinase (Syk) within 10 min, which led to endothelin-1 (ET-1) production. TLR4 was also rapidly activated by TNF-α stimulation, as shown by recruitment of interleukin-1 receptor-associated kinase 1 to TLR4 and its adaptor molecule, myeloid differentiation factor 88 (MyD88). siRNA depletion of TLR4 markedly attenuated TNF-α-induced Syk activation and ET-1 production. TLR4 inhibitor (CLI-095), TLR4-neutralizing antibody and siRNA depletion of MyD88 also attenuated TNF-α-induced Syk activation. Syk was co-immunoprecipitated with TLR4, and TNF-α activated Syk bound to TLR4. High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-α stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant. Glycyrrhizin (HMGB1 inhibitor), HMGB1-neutralizing antibody and siRNA depletion of HMGB1 all suppressed TNF-α-induced Syk activation and ET-1 production. Conclusion: Upon TNF-α stimulation, TLR4 is activated by HMGB1 that is immediately released after the generation of reactive oxygen species, and plays a crucial role in the signal transduction.

Liver X Receptor Activation Impairs Neutrophil Functions and Aggravates Sepsis

2019 ◽  
Vol 221 (9) ◽  
pp. 1542-1553 ◽  
Author(s):  
Fabrício O Souto ◽  
Fernanda V S Castanheira ◽  
Silvia C Trevelin ◽  
Braulio H F Lima ◽  
Guilherme Cesar Martelossi Cebinelli ◽  
...  
Keyword(s):  
Multiorgan Failure ◽  
Bacterial Load ◽  
Cecal Ligation ◽  
Neutrophil Infiltration ◽  
Receptor Activation ◽  
Messenger Ribonucleic Acid ◽  
X Receptors ◽  
Lxr Agonists

Abstract Background Liver X receptors (LXRs) are nuclear receptors activated by oxidized lipids and were previously implicated in several metabolic development and inflammatory disorders. Although neutrophils express both LXR-α and LXR-β, the consequences of their activation, particularly during sepsis, remain unknown. Methods We used the model of cecal ligation and puncture (CLP) to investigate the role of LXR activation during sepsis. Results In this study, we verified that LXR activation reduces neutrophil chemotactic and killing abilities in vitro. Mice treated with LXR agonists showed higher sepsis-induced mortality, which could be associated with reduced neutrophil infiltration at the infectious foci, increased bacteremia, systemic inflammatory response, and multiorgan failure. In contrast, septic mice treated with LXR antagonist showed increased number of neutrophils in the peritoneal cavity, reduced bacterial load, and multiorgan dysfunction. More important, neutrophils from septic patients showed increased ABCA1 messenger ribonucleic acid levels (a marker of LXR activation) and impaired chemotactic response toward CXCL8 compared with cells from healthy individuals. Conclusions Therefore, our findings suggest that LXR activation impairs neutrophil functions, which might contribute to poor sepsis outcome.

scholarly journals Acteoside improves survival in cecal ligation and puncture-induced septic mice via blocking of high mobility group box 1 release

2013 ◽  
Vol 35 (4) ◽  
pp. 348-354 ◽  
Author(s):  
Eun Sun Seo ◽  
Bo Kang Oh ◽  
Jhang Ho Pak ◽  
Soon-Ho Yim ◽  
Sangilyandi Gurunathan ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
High Mobility ◽  
High Mobility Group ◽  
Cecal Ligation And Puncture

scholarly journals High Mobility Group Box 1 Contributes to the Pathogenesis of Experimental Pulmonary Hypertension via Activation of Toll-like Receptor 4

2012 ◽  
Vol 18 (12) ◽  
pp. 1509-1518 ◽  
Author(s):  
Eileen M Bauer ◽  
Richard Shapiro ◽  
Han Zheng ◽  
Ferhaan Ahmad ◽  
David Ishizawar ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Mobility ◽  
High Mobility Group ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4
Sign in / Sign up

Export Citation Format

Share Document