Variation in lipid A structure in the pathogenic yersiniae

被引:220
作者
Rebeil, R
Ernst, RK
Gowen, BB
Miller, SI
Hinnebusch, BJ
机构
[1] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA
[2] Univ Washington, Dept Med, Seattle, WA 98195 USA
[3] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA
[4] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA
关键词
D O I
10.1111/j.1365-2958.2004.04059.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. After growth at 37degreesC, Y. pestis lipopolysaccharide (LPS) contained the tetra-acylated lipid IVA and smaller amounts of lipid IVA modified with C10 or C12 acyl groups, Y. pseudotuberculosis contained the same forms as part of a more heterogeneous population in which lipid IVA modified with C16:0 predominated, and Y. enterocolitica produced a unique tetra-acylated lipid A. When grown at 21degreesC, however, the three yersiniae synthesized LPS containing predominantly hexa-acylated lipid A. This more complex lipid A stimulated human monocytes to secrete tumour necrosis factor-alpha, whereas the lipid A synthesized by the three species at 37degreesC did not. The Y. pestis phoP gene was required for aminoarabinose modification of lipid A, but not for the temperature-dependent acylation changes. The results suggest that the production of a less immunostimulatory form of LPS upon entry into the mammalian host is a conserved pathogenesis mechanism in the genus Yersinia, and that species-specific lipid A forms may be important for life cycle and pathogenicity differences.
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页码:1363 / 1373
页数:11
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