NDLI: Decrease of Plasma Platelet-Activating Factor Acetylhydrolase Activity in Lipopolysaccharide Induced Mongolian Gerbil Sepsis Model

Content Provider	PubMed Central
Author	Yang, Junwei Xu, Jing Chen, Xiaoying Zhang, Yixuan Jiang, Xucheng Guo, Xiaokui Zhao, Guoping
Editor	Bereswill, Stefan
Abstract	Platelet-activating factor (PAF) plays an important role in the pathogenesis of sepsis, and the level of plasma PAF acetylhydrolase (pPAF-AH), which inactivates PAF, decreases in sepsis patients except for the sepsis caused by severe leptospirosis. Usually, increase of pPAF-AH activity was observed in lipopolysaccharide (LPS)-induced Syrian hamster and rat sepsis models, while contradictory effects were reported for mouse model in different studies. Here, we demonstrated the in vivo effects of LPS upon the change of pPAF-AH activity in C57BL/6 mice and Mongolian gerbils. After LPS-treatment, the clinical manifestations of Mongolian gerbil model were apparently similar to that of C57BL/6 mouse sepsis model. The pPAF-AH activity increased in C57BL/6 mice after LPS induction, but decreased in Mongolian gerbils, which was similar to that of the human sepsis. It thus suggests that among the LPS-induced rodent sepsis models, only Mongolian gerbil could be used for the study of pPAF-AH related to the pathogenesis of human sepsis. Proper application of this model might enable people to clarify the underline mechanism accounted for the contradictory results between the phase II and phase III clinical trials for the administration of recombinant human pPAF-AH in the sepsis therapy.
Related Links	http://dx.doi.org/10.1371/journal.pone.0009190
Starting Page	9190
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	2
Volume Number	5
Language	English
Publisher	Public Library of Science
Publisher Date	2010-02-12
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Platelet-activating factor acetylhydrolase activity in maternal, fetal, and newborn rabbit plasma during pregnancy and lactation.

Lipopolysaccharide and platelet-activating factor stimulate expression of platelet-activating factor acetylhydrolase via distinct signaling pathways

The Expression and Localization of Plasma Platelet-activating Factor Acetylhydrolase in Endotoxemic Rats

Lipoproteins alter the catalytic behavior of the platelet-activating factor acetylhydrolase in human plasma.

Elevated plasma phospholipase A2 and platelet-activating factor acetylhydrolase activity in colorectal cancer.

Deregulated platelet‐activating factor levels and acetylhydrolase activity in patients with idiopathic IgA nephropathy

Elevated plasma platelet-activating factor acetylhydrolase activity and its relationship to the presence of coronary artery disease*

Characterization of the platelet-activating factor acetylhydrolase from human plasma by heterologous expression in Xenopus laevis oocytes.

Lipopolysaccharide and platelet-activating factor stimulate expression of platelet-activating factor acetylhydrolase via distinct signaling pathways

Decrease of Plasma Platelet-Activating Factor Acetylhydrolase Activity in Lipopolysaccharide Induced Mongolian Gerbil Sepsis Model

Similar Documents

Platelet-activating factor acetylhydrolase activity in maternal, fetal, and newborn rabbit plasma during pregnancy and lactation.

Lipopolysaccharide and platelet-activating factor stimulate expression of platelet-activating factor acetylhydrolase via distinct signaling pathways

The Expression and Localization of Plasma Platelet-activating Factor Acetylhydrolase in Endotoxemic Rats

Lipoproteins alter the catalytic behavior of the platelet-activating factor acetylhydrolase in human plasma.

Elevated plasma phospholipase A2 and platelet-activating factor acetylhydrolase activity in colorectal cancer.

Deregulated platelet‐activating factor levels and acetylhydrolase activity in patients with idiopathic IgA nephropathy

Elevated plasma platelet-activating factor acetylhydrolase activity and its relationship to the presence of coronary artery disease*

Characterization of the platelet-activating factor acetylhydrolase from human plasma by heterologous expression in Xenopus laevis oocytes.

Lipopolysaccharide and platelet-activating factor stimulate expression of platelet-activating factor acetylhydrolase via distinct signaling pathways

Decrease of Plasma Platelet-Activating Factor Acetylhydrolase Activity in Lipopolysaccharide Induced Mongolian Gerbil Sepsis Model