Literature DB >> 11902292

Elevation of plasma peptidoglycan and peripheral blood neutrophil activation during hemorrhagic shock: plasma peptidoglycan reflects bacterial translocation and may affect neutrophil activation.

Tomoharu Shimizu1, Tohru Tani, Yoshihiro Endo, Kazuyoshi Hanasawa, Masakazu Tsuchiya, Masashi Kodama.   

Abstract

OBJECTIVE: To investigate the relations among bacterial transloation, plasma peptidoglycan elevation, and peripheral blood neutrophil activation during hemorrhagic shock.
DESIGN: Prospective, randomized, unblinded animal study.
SETTING: Surgical research laboratories of Shiga University of Medical Science.
SUBJECTS: Male, specific pathogen-free Sprague-Dawley rats.
INTERVENTIONS: The rats were randomly divided into three groups: a conventional group with normal intestinal flora (NF), an antibiotic (streptomycin and penicillin G) decontaminated group (AD), and a sham shock group with normal intestinal flora. The NF and AD groups were subjected to hemorrhagic shock (mean arterial pressure 30 mm Hg, for 30 to 90 mins). Rats were killed at 30, 60, and 90 mins after shock induction. Systemic blood and mesenteric lymph nodes (MLNs) were cultured for the determination of bacterial translocation (BT). Systemic plasma peptidoglycan and endotoxin concentrations were measured. To evaluate peripheral blood neutrophil activation, phagocytosis and hydrogen peroxide generation were assayed by flow cytometry.
MEASUREMENTS AND MAIN RESULTS: In the NF group, BT to MLNs was significantly increased from 30 mins after shock induction. Blood culture and plasma endotoxin were positive at 90 mins but there were no significant differences. Assayed plasma peptidoglycan was significantly increased at 90 mins. Phagocytosis and hydrogen peroxide generation were significantly increased. Assayed plasma peptidoglycan concentrations showed significant positive correlations with the magnitude of BT to MLNs (r2 = .54) and hydrogen peroxide generation (r2 = .22) in individual animals. Furthermore, BT and these parameters were significantly suppressed in the AD group.
CONCLUSIONS: First, we concluded that assayed plasma peptidoglycan reflects BT induced by hemorrhage because the increase in assayed plasma peptidoglycan was suppressed, as was BT, by antibiotic decontamination. Second, peripheral blood neutrophil activation was also suppressed when BT was prevented. We concluded BT to be involved in neutrophil activation. Our findings suggest hydrogen peroxide generation by neutrophils to be involved in plasma peptidoglycan elevation.

Entities:  

Mesh:

Substances:

Year:  2002        PMID: 11902292     DOI: 10.1097/00003246-200201000-00012

Source DB:  PubMed          Journal:  Crit Care Med        ISSN: 0090-3493            Impact factor:   7.598


  14 in total

Review 1.  Gut-liver axis in liver cirrhosis: How to manage leaky gut and endotoxemia.

Authors:  Hiroshi Fukui
Journal:  World J Hepatol       Date:  2015-03-27

2.  Triggering receptor expressed on myeloid cells-1 as a new therapeutic target during inflammatory diseases.

Authors:  Marc Derive; Frédéric Massin; Sébastien Gibot
Journal:  Self Nonself       Date:  2010-07-02

Review 3.  Endotoxemia-menace, marker, or mistake?

Authors:  Robert S Munford
Journal:  J Leukoc Biol       Date:  2016-07-14       Impact factor: 4.962

4.  Exogenous nitric oxide prevents cardiovascular collapse during hemorrhagic shock.

Authors:  Parimala Nachuraju; Adam J Friedman; Joel M Friedman; Pedro Cabrales
Journal:  Resuscitation       Date:  2011-02-20       Impact factor: 5.262

5.  Flutamide attenuates pro-inflammatory cytokine production and hepatic injury following trauma-hemorrhage via estrogen receptor-related pathway.

Authors:  Tomoharu Shimizu; Huang-Ping Yu; Ya-Ching Hsieh; Mashkoor A Choudhry; Takao Suzuki; Kirby I Bland; Irshad H Chaudry
Journal:  Ann Surg       Date:  2007-02       Impact factor: 12.969

6.  Organ injury and cytokine release caused by peptidoglycan are dependent on the structural integrity of the glycan chain.

Authors:  Anders E Myhre; Jon Fredrik Stuestøl; Maria K Dahle; Gunhild Øverland; Christoph Thiemermann; Simon J Foster; Per Lilleaasen; Ansgar O Aasen; Jacob E Wang
Journal:  Infect Immun       Date:  2004-03       Impact factor: 3.441

7.  Translocation of bacterial NOD2 agonist and its link with inflammation.

Authors:  Oh Yoen Kim; Antoine Monsel; Michèle Bertrand; Jean-Marc Cavaillon; Pierre Coriat; Minou Adib-Conquy
Journal:  Crit Care       Date:  2009-07-28       Impact factor: 9.097

8.  Extracorporeal immune therapy with immobilized agonistic anti-Fas antibodies leads to transient reduction of circulating neutrophil numbers and limits tissue damage after hemorrhagic shock/resuscitation in a porcine model.

Authors:  Tim T Lögters; Jens Altrichter; Adnana Paunel-Görgülü; Martin Sager; Ingo Witte; Annina Ott; Sarah Sadek; Jessica Baltes; José Bitu-Moreno; Alberto Schek; Wolfram Müller; Teresa Jeri; Joachim Windolf; Martin Scholz
Journal:  J Inflamm (Lond)       Date:  2010-04-20       Impact factor: 4.981

9.  Relations among circulating monocytes, dendritic cells, and bacterial translocation in patients with intestinal obstruction.

Authors:  Hisanori Shiomi; Tomoharu Shimizu; Yoshihiro Endo; Satoshi Murata; Yoshimasa Kurumi; Yoshitaka Uji; Tohru Tani
Journal:  World J Surg       Date:  2007-09       Impact factor: 3.352

10.  Selective inhibition of iNOS attenuates trauma-hemorrhage/resuscitation-induced hepatic injury.

Authors:  Wen-Hong Kan; Jun-Te Hsu; Martin G Schwacha; Mashkoor A Choudhry; Raghavan Raju; Kirby I Bland; Irshad H Chaudry
Journal:  J Appl Physiol (1985)       Date:  2008-07-17
View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.