Document Detail


Anti-IL-6 antibody treatment but not IL-6 knockout improves intestinal barrier function and reduces inflammation after binge ethanol exposure and burn injury.
MedLine Citation:
PMID:  23376955     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Interleukin 6 (IL-6) is an inflammatory cytokine known to be elevated in chronic diseases and after insults such as trauma and infection. Although necessary for the development of B cells and Th17 cells, IL-6, at elevated levels, can also cause tissue damage and lead to a rise in inflammation. Previous work in our laboratory has shown that IL-6 is increased both systemically and in multiple organ systems including the ileum after ethanol exposure and burn injury. As this combined insult causes elevated intestinal morphological damage, tight junction protein localization alterations, and phosphorylated myosin light chain levels, we sought to determine the role of IL-6 in these intestinal responses using a model of binge ethanol exposure and burn injury. Interleukin 6 antibody treatment after the combined insult reduced morphological changes in the ileum, bacterial translocation, and phosphorylated myosin light chain levels relative to either injury alone. Zonula occludens protein 1 and occludin localization was also reestablished in wild-type mice given IL-6 antibody after ethanol and burn. Interleukin 6-knockout mice given ethanol and burn injury also had reduced intestinal damage; however, no changes in bacterial translocation or tight junction protein localization were observed as compared with similarly treated wild-type mice. These data suggest that IL-6 may have a role in intestinal tissue damage observed after the combined insult of binge ethanol exposure and burn injury, although complete loss of IL-6 does not seem to be beneficial in this model. Modulation of IL-6 may present a new option for preventing intestinal damage and associated inflammation after a combined insult of ethanol exposure and burn injury.
Authors:
Anita Zahs; Melanie D Bird; Luis Ramirez; Mashkoor A Choudhry; Elizabeth J Kovacs
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  39     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-03-18     Completed Date:  2013-08-19     Revised Date:  2014-04-02    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  373-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / pharmacology*
Bacterial Translocation / drug effects,  immunology
Binge Drinking / immunology
Burns / physiopathology*
Cytokines / metabolism
Ethanol / toxicity*
Ileitis / chemically induced,  physiopathology,  prevention & control*
Interleukin-6 / antagonists & inhibitors,  deficiency,  immunology*
Mice
Mice, Inbred C57BL
Mice, Knockout
Myosin Light Chains / metabolism
Occludin / metabolism
Solvents / toxicity*
Zonula Occludens-1 Protein / metabolism
Grant Support
ID/Acronym/Agency:
F31 AA019913/AA/NIAAA NIH HHS; F31 AA019913/AA/NIAAA NIH HHS; F32 AA018068/AA/NIAAA NIH HHS; F32 AA018068/AA/NIAAA NIH HHS; P30 AA019373/AA/NIAAA NIH HHS; P30 AA019373/AA/NIAAA NIH HHS; R01 AA012034/AA/NIAAA NIH HHS; R01 AA012034/AA/NIAAA NIH HHS; T32 AA013527/AA/NIAAA NIH HHS; T32 AA013527/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies; 0/Cytokines; 0/Interleukin-6; 0/Myosin Light Chains; 0/Occludin; 0/Solvents; 0/Zonula Occludens-1 Protein; 3K9958V90M/Ethanol
Comments/Corrections

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


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