Endotoxemia

Publication Title: 
Journal of Pharmaceutical Sciences

Endotoxemia decreases the dose requirement for anesthetics but no data are available for propofol. A rat model was used in which the influence of endotoxin administration on the pharmacokinetics and pharmacodynamics of propofol was investigated. Chronically instrumented rats were randomly allocated to either a control (n = 9) or an endotoxin (n = 9) group. Six hours after pretreatment with either endotoxin or its solvent, propofol was infused (150 mg x kg(-1) x h(-1)) until isoelectric periods of 5 s or longer were observed in the electroencephalogram.

Author(s): 
De Paepe, Peter
Belpaire, Frans M.
Van Hoey, Gert
Boon, Paul A.
Buylaert, Walter A.
Publication Title: 
Acta Anaesthesiologica Taiwanica: Official Journal of the Taiwan Society of Anesthesiologists

BACKGROUND: Sepsis is characterized by an increase in nitric oxide (NO) production, hemodynamic dysfunction and multiple organ failure. Propofol, a commonly used anesthetic in the intensive care unit for sedation and hypnosis, is thought to exert a protective effect on NO overproduction by inhibiting the expression of inducible NO synthase (iNOS) in sepsis.

Author(s): 
Liu, Yen-Chin
Chan, Julie Y. H.
Tsai, Yu-Chuan
Publication Title: 
The British Journal of Nutrition

Amla (Emblica officinalis Gaertn.) has been used for many centuries in traditional Indian Ayurvedic formulations for the prevention and treatment of many inflammatory diseases. The present study evaluated the anti-inflammatory and anticoagulant properties of amla fruit extract. The amla fruit extract potentially and significantly reduced lipopolysaccharide (LPS)-induced tissue factor expression and von Willebrand factor release in human umbilical vein endothelial cells (HUVEC) in vitro at clinically relevant concentrations (1-100 μg/ml).

Author(s): 
Rao, Theertham Pradyumna
Okamoto, Takayuki
Akita, Nobuyuki
Hayashi, Tatsuya
Kato-Yasuda, Naomi
Suzuki, Koji
Publication Title: 
Medical Hypotheses

Despite recent advances in antibiotic therapy and intensive care, sepsis remains widespread problems in critically ill patients. The high mortality of sepsis is in part mediated by bacterial endotoxin, which stimulates macrophages/monocytes to sequentially release early (e.g., TNF, IL-1, and IFN-gamma) and late (e.g., HMGB1) pro-inflammatory cytokines.

Author(s): 
Chen, Xiaotian
Li, Wei
Wang, Haichao
Publication Title: 
The Journal of Nutrition

Despite recent advances in antibiotic therapy and intensive care, sepsis remains a widespread problem in critically ill patients. The high mortality from sepsis is in part mediated by bacterial endotoxin, which stimulates macrophages/monocytes to sequentially release early (e.g., tumor necrosis factor, interleukin-1, and interferon-gamma) and late [e.g., high mobility group box 1 protein (HMGB1)] proinflammatory cytokines. Our discovery of HMGB1 as a late mediator of lethal systemic inflammation has initiated a new field of investigation for the development of experimental therapeutics.

Author(s): 
Wang, Haichao
Li, Wei
Li, Jianhua
Rendon-Mitchell, Beatriz
Ochani, Mahendar
Ashok, Mala
Yang, Lihong
Yang, Huan
Tracey, Kevin J.
Wang, Ping
Sama, Andrew E.
Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

The pathogenesis of sepsis is mediated in part by bacterial endotoxin, which stimulates macrophages/monocytes to sequentially release early (e.g., TNF, IL-1, and IFN-gamma) and late (e.g., high mobility group box 1 (HMGB1) protein) proinflammatory cytokines. The recent discovery of HMGB1 as a late mediator of lethal sepsis has prompted investigation for development of new experimental therapeutics.

Author(s): 
Li, Wei
Li, Jianhua
Ashok, Mala
Wu, Rongqian
Chen, Dazhi
Yang, Lihong
Yang, Huan
Tracey, Kevin J.
Wang, Ping
Sama, Andrew E.
Wang, Haichao
Publication Title: 
Laboratory Investigation; a Journal of Technical Methods and Pathology

Endotoxemia participates in the pathogenesis of many liver injuries. Lipopolysaccharide (LPS) was shown to inactivate hepatic methionine adenosyltransferase (MAT), the enzyme responsible for S-adenosylmethionine (SAMe) biosynthesis. SAMe treatment was shown to prevent the LPS-induced increase in tumor necrosis factor-alpha, which may be one of its beneficial effects. SAMe is also an important precursor of glutathione (GSH) and GSH was shown to ameliorate LPS-induced hepatotoxicity.

Author(s): 
Ko, Kwangsuk
Yang, Heping
Noureddin, Mazen
Iglesia-Ara, Ainhoa
Xia, Meng
Wagner, Conrad
Luka, Zigmund
Mato, José M.
Lu, Shelly C.
Publication Title: 
Alcoholism, Clinical and Experimental Research

BACKGROUND: Clinical and animal data indicate that gut-derived endotoxin and other luminal bacterial products are necessary cofactors for development of alcoholic liver disease (ALD). Although gut leakiness is clearly an important cause of endotoxemia in ALD, it cannot fully explain endotoxemia in all ALD subjects and thus other factors may be involved. One possible factor is a change in gut microbiota composition (dysbiosis).

Author(s): 
Mutlu, Ece
Keshavarzian, Ali
Engen, Phillip
Forsyth, Christopher B.
Sikaroodi, Masoumeh
Gillevet, Patrick
Publication Title: 
PloS One

BACKGROUND: A liver-derived protein, fetuin-A, was first purified from calf fetal serum in 1944, but its potential role in lethal systemic inflammation was previously unknown. This study aims to delineate the molecular mechanisms underlying the regulation of hepatic fetuin-A expression during lethal systemic inflammation (LSI), and investigated whether alterations of fetuin-A levels affect animal survival, and influence systemic accumulation of a late mediator, HMGB1.

Author(s): 
Li, Wei
Zhu, Shu
Li, Jianhua
Huang, Yan
Zhou, Rongrong
Fan, Xuegong
Yang, Huan
Gong, Xing
Eissa, N. Tony
Jahnen-Dechent, Willi
Wang, Ping
Tracey, Kevin J.
Sama, Andrew E.
Wang, Haichao
Publication Title: 
Current Molecular Medicine

Infection and injury are two seemingly unrelated processes that often converge on common innate inflammatory responses mediated by pathogen- or damage-associated molecular patterns (PAMPs or DAMPs). If dysregulated, an excessive inflammation manifested by the overproduction and release of proinflammatory mediators (e.g., TNF, IFN-γ, and HMGB1) may adversely lead to many pathogenic consequences.

Author(s): 
Wang, H.
Sama, A. E.

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