scholarly journals Inducing Experimental Polymicrobial Sepsis by Cecal Ligation and Puncture

2020 ◽  
Vol 131 (1) ◽  
Author(s):  
Frances V. Sjaastad ◽  
Isaac J. Jensen ◽  
Roger R. Berton ◽  
Vladimir P. Badovinac ◽  
Thomas S. Griffith
Keyword(s):  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Cecal Ligation And Puncture

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 Blockade of the JNK Signalling as a Rational Therapeutic Approach to Modulate the Early and Late Steps of the Inflammatory Cascade in Polymicrobial Sepsis

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Gabriele Pizzino ◽  
Alessandra Bitto ◽  
Giovanni Pallio ◽  
Natasha Irrera ◽  
Federica Galfo ◽  
...  
Keyword(s):  
Therapeutic Approach ◽  
Caspase 3 ◽  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Sham Operation ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Cascade ◽  
Human Sepsis ◽  
Histopathologic Analysis ◽  
To Receive

Cecal ligation and puncture (CLP) is an experimental polymicrobial sepsis induced systemic inflammation that leads to acute organ failure. Aim of our study was to evaluate the effects of SP600125, a specific c-Jun NH2-terminal kinase (JNK) inhibitor, to modulate the early and late steps of the inflammatory cascade in a murine model of CLP-induced sepsis. CB57BL/6J mice were subjected to CLP or sham operation. Animals were randomized to receive either SP600125 (15 mg/kg) or its vehicle intraperitoneally 1 hour after surgery and repeat treatment every 24 hours. To evaluate survival, a group of animals was monitored every 24 hours for 120 hours. Two other animals were sacrificed 4 or 18 hours after surgical procedures; lung and liver samples were collected for biomolecular and histopathologic analysis. The expression of p-JNK, p-ERK, TNF-α, HMGB-1, NF-κB, Ras, Rho, Caspase 3, Bcl-2, and Bax was evaluated in lung and liver samples; SP600125 improved survival, reduced CLP induced activation of JNK, NF-κB, TNF-α, and HMGB-1, inhibited proapoptotic pathway, preserved Bcl-2 expression, and reduced histologic damage in both lung and liver of septic mice. SP600125 protects against CLP induced sepsis by blocking JNK signalling; therefore, it can be considered a therapeutic approach in human sepsis.

Transient Receptor Potential Melastatin 2 Protects Mice against Polymicrobial Sepsis by Enhancing Bacterial Clearance

2014 ◽  
Vol 121 (2) ◽  
pp. 336-351 ◽  
Author(s):  
XiaoWei Qian ◽  
Tomohiro Numata ◽  
Kai Zhang ◽  
CaiXia Li ◽  
JinChao Hou ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Knockout Mice ◽  
Transient Receptor Potential ◽  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Bacterial Clearance ◽  
Cecal Ligation And Puncture ◽  
Bacterial Burden ◽  
Wild Type ◽  
Transient Receptor Potential Melastatin

Abstract Background: Recent studies suggest that the transient receptor potential melastatin 2 (TRPM2) channel plays an important role in inflammation and immune response. However, the role and mechanism of TRPM2 in polymicrobial sepsis remain unclear. Methods: The authors explored the effects of genetic disruption of TRPM2 on mortality (n = 15), bacterial clearance (n = 6), organ injury, and systemic inflammation during cecal ligation and puncture–induced sepsis. Electrophysiology, immunoblot, bacterial clearance experiment, and quantitative real-time polymerase chain reaction were used to explore the role and mechanism of TRPM2 in sepsis. Results: After cecal ligation and puncture, Trpm2-knockout mice had increased mortality compared with wild-type mice (73.3 vs. 40%, P = 0.0289). The increased mortality was associated with increased bacterial burden, organ injury, and systemic inflammation. TRPM2-mediated Ca2+ influx plays an important role in lipopolysaccharide or cecal ligation and puncture–induced heme oxygenase-1 (HO-1) expression in macrophage. HO-1 up-regulation decreased bacterial burden both in wild-type bone marrow–derived macrophages and in cecal ligation and puncture–induced septic wild-type mice. Disruption of TRPM2 decreased HO-1 expression and increased bacterial burden in bone marrow–derived macrophages. Pretreatment of Trpm2-knockout bone marrow–derived macrophages with HO-1 inducer markedly increased HO-1 expression and decreased bacterial burden. Pretreatment of Trpm2-knockout mice with HO-1 inducer reversed the susceptibility of Trpm2-knockout mice to sepsis by enhancing the bacterial clearance. In addition, septic patients with lower monocytic TRPM2 and HO-1 messenger RNA levels had a worse outcome compared with septic patients with normal monocytic TRPM2 and HO-1 messenger RNA levels. TRPM2 levels correlated with HO-1 levels in septic patients (r = 0.675, P = 0.001). Conclusion: The study data demonstrate a protective role of TRPM2 in controlling bacterial clearance during polymicrobial sepsis possibly by regulating HO-1 expression.

The systemic inflammatory reaction in polymicrobial sepsis induced by murine cecal ligation and puncture is equally dependent on C5 and CD14

Immunobiology ◽  
2012 ◽  
Vol 217 (11) ◽  
pp. 1129
Author(s):  
Tom E. Mollnes ◽  
Andreas Barratt-Due ◽  
Søren E. Pischke ◽  
Øystein Sandanger ◽  
Miles A. Nunn ◽  
...  
Keyword(s):  
Inflammatory Reaction ◽  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Cecal Ligation And Puncture ◽  
Systemic Inflammatory Reaction

scholarly journals Poly(I:C) Priming Exacerbates Cecal Ligation and Puncture-Induced Polymicrobial Sepsis in Mice

Inflammation ◽  
2017 ◽  
Vol 41 (1) ◽  
pp. 328-336 ◽  
Author(s):  
Deepika Sharma ◽  
Ankit Malik ◽  
Nandakumar Packiriswamy ◽  
Michael D. Steury ◽  
Narayanan Parameswaran
Keyword(s):  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Poly I:C ◽  
Cecal Ligation And Puncture

scholarly journals PAD4-deficiency does not affect bacteremia in polymicrobial sepsis and ameliorates endotoxemic shock

Blood ◽  
2015 ◽  
Vol 125 (12) ◽  
pp. 1948-1956 ◽  
Author(s):  
Kimberly Martinod ◽  
Tobias A. Fuchs ◽  
Naamah L. Zitomersky ◽  
Siu Ling Wong ◽  
Melanie Demers ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
Polymicrobial Sepsis ◽  
Cecal Ligation And Puncture ◽  
Key Points ◽  
Endotoxemic Shock ◽  
Improved Outcome

Key Points Absence of NETs in PAD4−/− mice did not affect bacteremia in polymicrobial sepsis produced by cecal ligation and puncture. PAD4-deficiency improved outcome in lipopolysaccharide (LPS)-induced sepsis.

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