{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,5,2]],"date-time":"2023-05-02T22:10:09Z","timestamp":1683065409040},"reference-count":41,"publisher":"Microbiology Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,5,1]]},"abstract":"<jats:p>To study the possible mechanism of extracellular resistance to phagocytes developed by<jats:italic>Yersinia pestis<\/jats:italic>in the early stage of plague infection, the behaviour of two<jats:italic>Y. pestis<\/jats:italic>strains, the vaccine EV-76 and fully virulent 231 (LD<jats:sub>50<\/jats:sub>, 10 c.f.u.), was studied in-depth after cultivation<jats:italic>in vitro<\/jats:italic>at the host temperature in conditions simulating the bloodstream environment of mammals. For this, two standard basal media supplemented with calcium and glucose in appropriate concentrations were employed: Hottinger broth, routinely used for growth of<jats:italic>Y. pestis in vitro<\/jats:italic>, and RPMI 1640, simulating human extracellular fluid. Although both media permitted<jats:italic>Y. pestis<\/jats:italic>to achieve the resistant state, RPMI enabled significantly higher bacterial proliferation and increased modifications in the production of the principal surface antigens that affect the relevant phenotype characteristics. In general, our results indicate that the<jats:italic>Y. pestis<\/jats:italic>bacteria in the resistant state do not produce species-specific antigens, i.e. fraction 1 or F1, \u2018murine\u2019 toxin or Ymt, plasminogen activator (Pla) and any surface-specific polysaccharides, resulting in unmasking of the cross-reactive epitopes of lipid A in reduced<jats:italic>Y. pestis<\/jats:italic>lipopolysaccharide. This may produce mimicry by<jats:italic>Y. pestis<\/jats:italic>of some human tissue and blood cell components, with no immune response and inflammation at the site of infection at the early stage, which enables<jats:italic>Y. pestis<\/jats:italic>to survive, extensively multiply and spread into the circulation.<\/jats:p>","DOI":"10.1099\/jmm.0.45932-0","type":"journal-article","created":{"date-parts":[[2005,4,11]],"date-time":"2005-04-11T23:38:02Z","timestamp":1113262682000},"page":"435-441","source":"Crossref","is-referenced-by-count":8,"title":["Antigenic and phenotypic modifications of Yersinia pestis under calcium and glucose concentrations simulating the mammalian bloodstream environment"],"prefix":"10.1099","volume":"54","author":[{"given":"Valentina A","family":"Feodorova","sequence":"first","affiliation":[{"name":"Laboratory of Hybridomas, Russia State Antiplague Research Institute \u2018Microbe', Saratov, Universitetskaya, 46, Saratov, 410005, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alina B","family":"Golova","sequence":"additional","affiliation":[{"name":"Laboratory of Hybridomas, Russia State Antiplague Research Institute \u2018Microbe', Saratov, Universitetskaya, 46, Saratov, 410005, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"345","reference":[{"key":"H1-3","first-page":"12","article-title":"Somatic polysaccharide-containing antigens of Pasteurella pestis","volume":"3","author":"Bakhrakh","year":"1972","journal-title":"Zh Mikrobiol Epidemiol Immunobiol"},{"key":"H2-3","doi-asserted-by":"crossref","first-page":"6564","DOI":"10.1128\/JB.181.20.6564-6568.1999","article-title":"The modality of enterobacterial common antigen polysaccharide chain lengths is regulated by o349 of the wec gene cluster of Escherichia coli K-12","volume":"181","author":"Barr","year":"1999","journal-title":"J Bacteriol"},{"key":"H3-3","doi-asserted-by":"crossref","first-page":"19","DOI":"10.1128\/JB.94.1.19-26.1967","article-title":"Pesticins.III. 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