Zuckerzusammensetzung des Lipopolysaccharids und Feinstruktur der äußeren Membran (Zellwand) bei Yersinia enterocolitica

Acker, Georg; Wartenberg, Klaus; Knapp, W.

doi:10.1016/s0172-5599(80)80008-3

Cited by 10 publications

(4 citation statements)

References 19 publications

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“…Nonspecific fixation of complement to gram-negative bacteria can often be prevented by lipopolysaccharide (2,25,37), but little is known about the structures that account for serum resistance. In this context, it is probably significant that the predominant sugars in 0groups of many Y. enterocolitica serotypes are deoxyhexoses (30,48), whereas those of Y. pseudotuberculosis contain even more hydrophobic dideoxyhexoses (18,42); profound temperature-dependent changes in Y. enterocolitica 0-group content have been described (1,27).…”

Section: Resultsmentioning

confidence: 99%

Vwa+ phenotype of Yersinia enterocolitica

Perry¹,

Brubaker²

1983

Infect Immun

109

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Expression of the Vwa+ phenotype of Yersinia pestis in vitro is known to reflect maximum induction of virulence (or V and W antigens) at 37°C with concomitant restriction of cell division. Both phenomena are potentiated by 20 mM Mg2' and prevented by cultivation at 26 or 37°C with 2.5 mM Ca2+. We have now compared this classic plasmid-mediated phenotype with those of Vwa+ Yersinia pseudotuberculosis and Yersinia enterocolitica which, unlike Y. pestis, produce ancillary outer membrane peptides unrelated to the V and W antigens. All of 10 wild-type strains of Y. enterocolitica (serotypes 0:3, 0:4,32, 0:8, 0:9, 0:15, and 0:21) exhibited a nutritional requirement for Ca2' at 37°C and produced significant V antigen. Like Y. pseudotuberculosis, autoagglutination of Vwa+ Y. enterocolitica was dependent upon prior growth at 37°C but was not influenced by Ca2?. Autoagglutination of Y. pestis was never observed. Resistance of Y. enterocolitica to 10% human serum was typically dependent upon prior growth at 37°C, either with or without added Ca2', and carriage of a Vwa plasmid. In contrast, serum resistance of Y. pseudotuberculosis was temperature but not plasmid dependent and that of Y. pestis was constitutive. Many of the more severe bacterial diseases of man are caused by facultative intracellular parasites (38). Yersinia pestis, the causative agent of bubonic plague, is considered the type species of this group by virtue of its classical role in identifying virulence factors required for extracellular growth (8, 10). However, the most important determinant of this species is the ability to promote maximum expression (9) of the V and W (or virulence) antigens (Vwa+) of Burrows and Bacon (11), a property possibly required for intracellular survival. Mutation to Vwa-in Y. pestis results in a 106to 107-fold increase in the 50% lethal dose in experimental animals (10). V antigen is a 90-megadalton (mDal) protein and W antigen is a 140 mDal lipoprotein (35). Their synthesis is coordinately induced at 37 but not 26°C in synthetic medium simulating intraleukocytic fluid with respect to Ca2+ (not added) and Mg2+ (-20 mM). This environment selectively prevents in vitro division of Vwa+ cells; addition of that concentration of Ca2+ present in plasma (-2.5 mM) permits growth while coordinately repressing the V and W antigens (8). Recent work showed that restriction promoted by Ca>2 deprivation is a consequence of an ordered stepdown of macromolecular synthesis initiated by reduction of adenylate energy charge and shutoff of stable RNA synthesis (16, t Journal article no. 10633 from the Michigan Agricultural Experiment Station.

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Section: Resultsmentioning

confidence: 99%

Vwa+ phenotype of Yersinia enterocolitica

Perry¹,

Brubaker²

1983

Infect Immun

109

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“…LPS of Y. pseudotuberculosis grown at 37°C is similarly rough, whereas that isolated after incubation at 26°C possesses short 0-group side chains containing the hydrophobic serodominant 3,6-dideoxyhexoses abequose, ascarylose, colitose, paratose, and tyvelose (50, 131). Y. enterocolitica exhibits a more typical enteric LPS structure containing long 0-group side chains which, however, may also be enriched or exclusively composed of hydrophobic sugars (1,77,117). Endotoxicity of LPS from Y. pestis (2) and probably that of the enteropathogenic yersiniae are comparable to preparations from other enteric species.…”

Section: Lpsmentioning

confidence: 99%

Factors promoting acute and chronic diseases caused by yersiniae

1991

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The experimental system constructed with the medically significant yersiniae provides a powerful basic model for comparative study of factors required for expression of acute versus chronic disease. The system exploits the close genetic similarity between Yersinia pestis, the etiological agent of bubonic plague, and enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica. Y. pestis possesses three plasmids, of which one, shared by the enteropathogenic species, mediates a number of virulence factors that directly or indirectly promote survival within macrophages and immunosuppression. The two remaining plasmids are unique and encode functions that promote acute disease by enhancing bacterial dissemination in tissues and resistance to phagocytosis by neutrophils and monocytes. These properties are replaced in the enteropathogenic yersiniae by host cell invasins and an adhesin which promote chronic disease; the latter are cryptic in Y. pestis. Additional distinctions include specific mutational losses in Y. pestis which result in loss of fitness in natural environments plus gain of properties that facilitate transmission and infection via fleabite.

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“…This demonstration of rough LPS is in accordance with prior findings of others reported for Y. pestis 43,44 and for Y. enterocolitica (of serotypes other than 0:8, following growth at 37°C but not room temperature. [45][46][47][48] No significant temperature-dependent differences were noted between LPS structure of serotype 0:8 cells of Y. enterocolitica. Further study will be required to determine if the 6 h period of adaptation at 37°C used in the present study was insufficient to promote alteration of LPS structure or if retention of smooth configuration at 37°C reflects differences in serotype.…”

Section: It Is Evident From Comparison Of the Variables Listed Inmentioning

confidence: 99%

Lipopolysaccharide-associated resistance to killing of yersiniae by complement

Porat

McCabe

Brubaker

1995

Journal of Endotoxin Research

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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 Ca 2+ (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 51 Cr 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. pseudotuberculosis 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.Virulence factors encoded on a -70 kb low calcium response (Lcr) plasmid shared by Yersinia pestis, the causative agent of bubonic plague, and closely related enteropathogenic yersiniae (Y. enterocolitica and Y. pseudotuberculosis) are expressed in medium simulating mammalian cytoplasm with respect to Ca2+ z 0.1 1 mM), Mg2+ (-20 mM), and temperature (-37°C).~Ĩ mportant examples include secreted anti-inflammatory V antigen4 and the cytotoxic peptides YpkA,S YopE,6 and Y opH 7 which, in the case of Y. pestis, undergo prompt posttranslational degradation ' unless delivered to host cell cytoplasm by a process requiring bacterial contract. 12 Mutational loss of any one of these determinants causes the intravenous mouse 50% lethal dose to increase from < 102 to > 10 7 bacteria. 5,13-15 In addition, the Lcr plasmid encodes regulatory functions that mediate the low calcium response plus a number of minor determinants of pathogenicity where mutational loss results in a more modest reduction in virulence (mouse intravenous 50% lethal dose < 106 bacteria).l3

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Zuckerzusammensetzung des Lipopolysaccharids und Feinstruktur der äußeren Membran (Zellwand) bei Yersinia enterocolitica

Cited by 10 publications

References 19 publications

Vwa+ phenotype of Yersinia enterocolitica

Vwa+ phenotype of Yersinia enterocolitica

Factors promoting acute and chronic diseases caused by yersiniae

Lipopolysaccharide-associated resistance to killing of yersiniae by complement

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