| The lipid A phosphate position determines differential host Toll-like receptor 4 responses to phylogenetically related symbiotic and pathogenic bacteria. | |
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MedLine Citation:
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PMID: 20974832 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The human symbiont Bacteroides thetaiotaomicron promotes intestinal function and health, whereas the phylogenetically related pathogen Porphyromonas gingivalis is associated with the chronic oral inflammatory disease periodontitis. Although both B. thetaiotaomicron and P. gingivalis synthesize lipopolysaccharides (LPS) consisting of penta-acylated, monophosphorylated lipid A in addition to immunologically silent, nonphosphorylated lipid A, they elicit strikingly distinct Toll-like receptor 4 (TLR4) responses. We show that the phosphate position of penta-acylated, monophosphorylated lipid A is a key feature for determining the differential TLR4 responses elicited by these evolutionarily related bacteria. B. thetaiotaomicron produces TLR4-stimulatory lipid A bearing a 1-phosphate, in contrast to P. gingivalis, which produces TLR4-evasive lipid A bearing a 4'-phosphate. Confirming these observations, recombinant Escherichia coli LPS containing penta-acylated, 1-phosphorylated lipid A is more TLR4 stimulatory than LPS containing 4'-phosphorylated lipid A. The specific capacity of a Gram-negative bacterium to alert or evade the host innate immune defense system through TLR4-dependent signaling is currently recognized as a critical aspect defining the relationship between the host and the bacterium. We propose that the distinct lipid A phosphate positions observed for the B. thetaiotaomicron and P. gingivalis LPS contributes to the manifestation of these bacteria as commensal or pathogen within the human host. |
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Authors:
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Stephen R Coats; Alex B Berezow; Thao T To; Sumita Jain; Brian W Bainbridge; Karim P Banani; Richard P Darveau |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-10-25 |
Journal Detail:
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Title: Infection and immunity Volume: 79 ISSN: 1098-5522 ISO Abbreviation: Infect. Immun. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-23 Completed Date: 2011-01-25 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 0246127 Medline TA: Infect Immun Country: United States |
Other Details:
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Languages: eng Pagination: 203-10 Citation Subset: IM |
Affiliation:
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Department of Periodontics, School of Dentistry, University of Washington, 1959 NE Pacific St., HSB, Box 357444, Seattle, WA 98195, USA. scoats@u.washington.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Bacteroides
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genetics*,
metabolism Carbohydrate Conformation Escherichia coli / genetics*, metabolism Gene Expression Regulation / physiology HEK293 Cells Host-Pathogen Interactions Humans Lipid A / chemistry*, metabolism Phylogeny Porphyromonas gingivalis / genetics*, metabolism Symbiosis Toll-Like Receptor 4 / genetics, metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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DE012768/DE/NIDCR NIH HHS; DE018274/DE/NIDCR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Lipid A; 0/TLR4 protein, human; 0/Toll-Like Receptor 4 |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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