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Lipopolysaccharide-associated resistance to killing of yersiniae by complement

Division of Geographic Medicine and Infectious Diseases, New England Medical Center, Boston, MA, The Maxwell Finland Laboratory for Infectious Diseases, Boston University School of Medicine, Boston, MA, Department of Microbiology, Michigan State University, East Lansing, MI, USA

W.R. McCabe

Division of Geographic Medicine and Infectious Diseases, New England Medical Center, Boston, MA, The Maxwell Finland Laboratory for Infectious Diseases, Boston University School of Medicine, Boston, MA, Department of Microbiology, Michigan State University, East Lansing, MI, USA

R.R. Brubaker

Division of Geographic Medicine and Infectious Diseases, New England Medical Center, Boston, MA, The Maxwell Finland Laboratory for Infectious Diseases, Boston University School of Medicine, Boston, MA, Department of Microbiology, Michigan State University, East Lansing, MI, USA

Yersinia pestis, Y. pseudotuberculosis, and Y. enterocolitica share ~70 kb low calcium response (Lcr) plasmids encoding virulence factors expressed at 37°C that, except for the adhesin YadA, are repressed by Ca²⁺ (Lcr⁺). Virulence factors encoded on both the Lcr plasmid and chromosome have been reported to protect yersiniae against complement-dependent killing. In this study, LPS was isolated from yersiniae of serum-sensitive phenotypes (Lcr⁺ and Lcr^- Y. enterocolitica and Y. pseudotuberculosis grown at 26°C and Lcr ^- Y. enterocolitica grown at 37°C) and incorporated into liposomes containing radioactive chromium. These vesicles lysed with release of free ⁵¹Cr in normal but not decomplemented serum. Liposomes prepared from serum-resistant phenotypes (Lcr⁺ and Lcr^- Y. pestis grown at 26°C or 37°C, Lcr⁺ and Lcr^- Y. pseudotubercu losis grown at 37°C, and Lcr⁺ Y. enterocolitica grown at 37°C) did not undergo complement-dependent lysis. LPS from serum-resistant Y. pestis and Y. pseudotuberculosis was rough as judged by deficiency of O-groups.

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