Document Detail


The endogenous bacteria alter gut epithelial apoptosis and decrease mortality following Pseudomonas aeruginosa pneumonia.
MedLine Citation:
PMID:  23042193     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The endogenous bacteria have been hypothesized to play a significant role in the pathophysiology of critical illness, although their role in sepsis is poorly understood. The purpose of this study was to determine how commensal bacteria alter the host response to sepsis. Conventional and germ-free (GF) C57Bl/6 mice were subjected to Pseudomonas aeruginosa pneumonia. All GF mice died within 2 days, whereas 44% of conventional mice survived for 7 days (P = 0.001). Diluting the dose of bacteria 10-fold in GF mice led to similar survival in GF and conventional mice. When animals with similar mortality were assayed for intestinal integrity, GF mice had lower levels of intestinal epithelial apoptosis but similar levels of proliferation and intestinal permeability. Germ-free mice had significantly lower levels of tumor necrosis factor and interleukin 1β in bronchoalveolar lavage fluid compared with conventional mice without changes in systemic cytokine production. Under conventional conditions, sepsis unmasks lymphocyte control of intestinal epithelial apoptosis, because sepsis induces a greater increase in gut apoptosis in Rag-1 mice than in wild-type mice. However, in a separate set of experiments, gut apoptosis was similar between septic GF Rag-1 mice and septic GF wild-type mice. These data demonstrate that the endogenous bacteria play a protective role in mediating mortality from pneumonia-induced sepsis, potentially mediated through altered intestinal apoptosis and the local proinflammatory response. In addition, sepsis-induced lymphocyte-dependent increases in gut epithelial apoptosis appear to be mediated by the endogenous bacteria.
Authors:
Amy C Fox; Kevin W McConnell; Benyam P Yoseph; Elise Breed; Zhe Liang; Andrew T Clark; David O'Donnell; Brendan Zee-Cheng; Enjae Jung; Jessica A Dominguez; W Michael Dunne; Eileen M Burd; Craig M Coopersmith
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  38     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-18     Completed Date:  2013-03-11     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  508-14     Citation Subset:  IM    
Affiliation:
Department of Surgery, Washington University School of Medicine, St Louis, MO, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Germ-Free Life*
Intestinal Mucosa / metabolism*,  microbiology*,  pathology
Mice
Mice, Knockout
Pneumonia, Bacterial / genetics,  metabolism*,  pathology
Pseudomonas Infections / genetics,  metabolism*,  pathology
Pseudomonas aeruginosa*
Sepsis / genetics,  metabolism,  microbiology,  pathology
Grant Support
ID/Acronym/Agency:
DK52574/DK/NIDDK NIH HHS; GM008795/GM/NIGMS NIH HHS; GM072808/GM/NIGMS NIH HHS; GM095442/GM/NIGMS NIH HHS; GM66202/GM/NIGMS NIH HHS; P30 DK052574/DK/NIDDK NIH HHS; R01 GM066202/GM/NIGMS NIH HHS; R01 GM072808/GM/NIGMS NIH HHS; T32 GM008795/GM/NIGMS NIH HHS; T32 GM095442/GM/NIGMS NIH HHS
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