Biological relevance of lipid A variation in Yersinia spp
Important pathogens in the genus Yersinia include the plague bacillus Yersinia pestis and two enteropathogenic species, Yersinia pseudotuberculosis and Yersinia enterocolitica. A shift in growth temperature induced changes in the number and type of acyl groups on the lipid A of all three species. At...
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Published in | Journal of endotoxin research Vol. 10; no. 5; p. 6 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
01.01.2004
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Subjects | |
Online Access | Get full text |
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Summary: | Important pathogens in the genus Yersinia include the plague bacillus Yersinia pestis and two enteropathogenic species, Yersinia pseudotuberculosis and Yersinia enterocolitica. A shift in growth temperature induced changes in the number and type of acyl groups on the lipid A of all three species. At a temperature that mimics growth with the flea (21 degree C), Y. pestis synthesized a hexa-acylated lipid A molecule that was modified by a C16:1 fatty acid acyl group. In contrast, after growth at mammalian body temperatures (37 degree C) Y. pestis produced predominately tetra- and penta-acylated lipid A structures. Specifically, Y. pestis lipid A consisted of lipid IV sub(A) (a disaccharide precursor of lipid A) and smaller amounts of penta-acylated lipid A structures modified by the addition of either C10:0 or C12:0 fatty acid acyl groups. In contrast, Y. pseudotuberculosis primarily synthesized lipid IV sub(A) modified with C16:0, and Y. enterocolitica produced a unique tetra-acylated lipid A. The acyltransferase genes (htrB and lpxP) required for increased acylation at 21 degree C have been determined. The more complex lipid A made by the three species at 21 degree C stimulated human monocytes to secrete TNF- alpha , but lipid A synthesized at 37 degree C did not. Finally, the Y. pestis phoP gene was required for aminoarabinose modification of lipid A but not for the temperature-dependent acylation changes. Production of a less immunostimulatory form of LPS upon entry into the mammalian host appears to be a conserved pathogenesis mechanism in the genus Yersinia, and species-specific lipid A forms may be important for life cycle and pathogenicity differences. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-2 content type line 23 SourceType-Conference Papers & Proceedings-1 ObjectType-Conference-3 ObjectType-Feature-1 |
ISSN: | 0968-0519 |