| The endogenous bacteria alter gut epithelial apoptosis and decrease mortality following Pseudomonas aeruginosa pneumonia. | |
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MedLine Citation:
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PMID: 23042193 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Shock (Augusta, Ga.) Volume: 38 ISSN: 1540-0514 ISO Abbreviation: Shock Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-10-18 Completed Date: 2013-03-11 Revised Date: 2013-04-23 |
Medline Journal Info:
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Nlm Unique ID: 9421564 Medline TA: Shock Country: United States |
Other Details:
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Languages: eng Pagination: 508-14 Citation Subset: IM |
Affiliation:
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Department of Surgery, Washington University School of Medicine, St Louis, MO, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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