抄録
<jats:title>Summary</jats:title><jats:p>Important pathogens in the genus <jats:italic>Yersinia</jats:italic> include the plague bacillus <jats:italic>Yersinia pestis</jats:italic> and two enteropathogenic species, <jats:italic>Yersinia pseudotuberculosis</jats:italic> and <jats:italic>Yersinia enterocolitica</jats:italic>. 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 37°C, <jats:italic>Y. pestis</jats:italic> lipopolysaccharide (LPS) contained the tetra‐acylated lipid IV<jats:sub>A</jats:sub> and smaller amounts of lipid IV<jats:sub>A</jats:sub> modified with C10 or C12 acyl groups, <jats:italic>Y. pseudotuberculosis</jats:italic> contained the same forms as part of a more heterogeneous population in which lipid IV<jats:sub>A</jats:sub> modified with C16:0 predominated, and <jats:italic>Y. enterocolitica</jats:italic> produced a unique tetra‐acylated lipid A. When grown at 21°C, 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‐α, whereas the lipid A synthesized by the three species at 37°C did not. The <jats:italic>Y. pestis phoP</jats:italic> 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 <jats:italic>Yersinia</jats:italic>, and that species‐specific lipid A forms may be important for life cycle and pathogenicity differences.</jats:p>
収録刊行物
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- Molecular Microbiology
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Molecular Microbiology 52 (5), 1363-1373, 2004-04-28
Wiley
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詳細情報 詳細情報について
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- CRID
- 1363951794594027904
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- NII論文ID
- 80016726843
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- ISSN
- 13652958
- 0950382X
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