{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T13:52:20Z","timestamp":1761918740054},"reference-count":43,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2005,10,6]],"date-time":"2005-10-06T00:00:00Z","timestamp":1128556800000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The Lyme disease\u2010pathogen <jats:italic>Borrelia burgdorferi<\/jats:italic> binds the complement inhibitor factor H (FH) to its outer surface protein E\u2010 (OspE) and BbA68\u2010families of lipoproteins. In earlier studies, only serum\u2010resistant strains of the genospecies <jats:italic>B. burgdorferi<\/jats:italic> sensu stricto or <jats:italic>B. afzelii<\/jats:italic>, but not serum\u2010sensitive <jats:italic>B. garinii<\/jats:italic> strains, have been shown to bind FH. Since <jats:italic>B. garinii<\/jats:italic> often causes neuroborreliosis in man, we have readdressed the interactions of <jats:italic>B. garinii<\/jats:italic> with FH. <jats:italic>B. garinii<\/jats:italic> 50\/97 strain did not express FH\u2010binding proteins. By transforming the <jats:italic>B. garinii<\/jats:italic> 50\/97 strain with an OspE\u2010encoding gene from complement\u2010resistant <jats:italic>B. burgdorferi<\/jats:italic> (<jats:italic>ospE\u2010297<\/jats:italic>), its resistance to serum killing could be increased. <jats:italic>OspE gene<\/jats:italic>s were detected and cloned from the <jats:italic>B. garinii <\/jats:italic>BITS, Pistoia and 40\/97 strains by PCR and sequencing. The deduced amino acid sequences differed in an N\u2010terminal lysine\u2010rich FH\u2010binding region from OspE sequences of resistant strains. Recombinant <jats:italic>B. garinii<\/jats:italic> BITS OspE protein was found to have a considerably lower FH\u2010binding activity than the <jats:italic>B. burgdorferi<\/jats:italic> sensu stricto 297 OspE protein P21 (P21\u2013297). Unlike bacteria that had been kept in culture for a long time, neurovirulent <jats:italic>B. garinii<\/jats:italic> strains from neuroborreliosis patients were found to express \u223c27\u2010kDa FH\u2010binding proteins. These were not recognized by polyclonal anti\u2010OspE or anti\u2010BbA68 antibodies. We conclude that <jats:italic>B. garinii<\/jats:italic> strains carry <jats:italic>ospE<\/jats:italic> genes but have a decreased expression of OspE proteins and a reduced ability to bind FH, especially when grown for prolonged periods <jats:italic>in vitro<\/jats:italic>. Recently isolated neuroinvasive <jats:italic>B. garinii<\/jats:italic> strains, however, can express FH\u2010binding proteins, which may contribute to the virulence of neuroborreliosis\u2010causing <jats:italic>B. garinii<\/jats:italic> strains.<\/jats:p>","DOI":"10.1002\/eji.200526354","type":"journal-article","created":{"date-parts":[[2005,10,6]],"date-time":"2005-10-06T11:19:41Z","timestamp":1128597581000},"page":"3043-3053","source":"Crossref","is-referenced-by-count":50,"title":["Expression of complement factor H binding immunoevasion proteins in <i>Borrelia garinii <\/i>isolated from patients with neuroborreliosis"],"prefix":"10.1002","volume":"35","author":[{"given":"Antti","family":"Alitalo","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Taru","family":"Meri","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P\u00e4r","family":"Comstedt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luke","family":"Jeffery","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johanna","family":"Tornberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomas","family":"Strandin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hilkka","family":"Lankinen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sven","family":"Bergstr\u00f6m","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marina","family":"Cinco","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Santosh\u2004R.","family":"Vuppala","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darrin\u2004R.","family":"Akins","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seppo","family":"Meri","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,10,6]]},"reference":[{"key":"e_1_2_7_1_2","doi-asserted-by":"publisher","DOI":"10.1093\/clinids\/17.4.708"},{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.69.6.3685-3691.2001"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004300050038"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200106)31:6<1674::AID-IMMU1674>3.0.CO;2-2"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410400408"},{"key":"e_1_2_7_6_2","first-page":"19","article-title":"Role of complement in inflammation and injury in the nervous system.","volume":"14","author":"Morgan B. 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