Document Detail


Epigenetic regulation of immune cell functions during post-septic immunosuppression.
MedLine Citation:
PMID:  21048427     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Studies in humans and animal models indicate that profound immunosuppression is one of the chronic consequences of severe sepsis. This immune dysfunction encompasses deficiencies in activation of cells in both the myeloid and lymphoid cell lineages. As a result, survivors of severe sepsis are at risk of succumbing to infections perpetrated by opportunistic pathogens that are normally controlled by a fully functioning immune system. Recent studies have indicated that epigenetic mechanisms may be one driving force behind this immunosuppression, through suppression of proinflammatory gene production and subsequent immune cell activation, proliferation and effector function. A better understanding of epigenetics and post-septic immunosuppression can improve our diagnostic tools and may be an important potential source of novel molecular targets for new therapies. This review will discuss important pathways of immune cell activation affected by severe sepsis, and highlight pathways of epigenetic regulation that may be involved in post-septic immunosuppression.
Authors:
William F Carson; Karen A Cavassani; Yali Dou; Steven L Kunkel
Related Documents :
20691987 - Dehydroepiandrosterone during sepsis: does the timing of administration influence the e...
10786967 - Leukocytes: friend or foe.
1540097 - Does endotoxin tolerance prevent the release of inflammatory monokines (interleukin 1, ...
10897267 - Inflammatory responses and mediators.
15069387 - Innate immunity and toll-like receptors: clinical implications of basic science research.
21752117 - The neuropeptide calcitonin gene-related peptide affects allergic airway inflammation b...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-03-01
Journal Detail:
Title:  Epigenetics : official journal of the DNA Methylation Society     Volume:  6     ISSN:  1559-2308     ISO Abbreviation:  Epigenetics     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-03-23     Completed Date:  2011-07-22     Revised Date:  2011-10-28    
Medline Journal Info:
Nlm Unique ID:  101265293     Medline TA:  Epigenetics     Country:  United States    
Other Details:
Languages:  eng     Pagination:  273-83     Citation Subset:  IM    
Affiliation:
Department of Pathology, University of Michigan, Ann Arbor, USA. wfcarson@umich.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Proliferation
Epigenesis, Genetic*
Humans
Immune Tolerance / genetics*
Immunity, Innate / genetics
Models, Biological
Sepsis / genetics*,  immunology*
Grant Support
ID/Acronym/Agency:
HL089216/HL/NHLBI NIH HHS; HL31237/HL/NHLBI NIH HHS; R01 HL031237-27/HL/NHLBI NIH HHS
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cystic fibrosis: a disorder with defective autophagy.
Next Document:  Extracellular matrix-derived peptides and myocardial repair.