Variation in lipid A structure in the pathogenic yersiniae
Molecular microbiology, 2004•Wiley Online Library
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 37° C, 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 …
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 37° C, 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 …
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. After growth at 37°C, 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 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 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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