<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0872-8178</journal-id>
<journal-title><![CDATA[Jornal Português de Gastrenterologia ]]></journal-title>
<abbrev-journal-title><![CDATA[J Port Gastrenterol.]]></abbrev-journal-title>
<issn>0872-8178</issn>
<publisher>
<publisher-name><![CDATA[Sociedade Portuguesa de Gastrenterologia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0872-81782006000600001</article-id>
<title-group>
<article-title xml:lang="pt"><![CDATA[Avaliação do potencial patogénico dos genes sabA e hopZ de estirpes de Helicobacter Pylori isoladas numa população portuguesa]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Carvalho]]></surname>
<given-names><![CDATA[A.]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Oleastro]]></surname>
<given-names><![CDATA[M.]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Nunes]]></surname>
<given-names><![CDATA[B.]]></given-names>
</name>
<xref ref-type="aff" rid="A02"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Monteiro]]></surname>
<given-names><![CDATA[L.]]></given-names>
</name>
</contrib>
</contrib-group>
<aff id="A01">
<institution><![CDATA[,Instituto Nacional de Saúde Dr. Ricardo Jorge Centro de Bacteriologia Unidade de Helicobacter/Campylobacter]]></institution>
<addr-line><![CDATA[Lisboa ]]></addr-line>
<country>Portugal</country>
</aff>
<aff id="A02">
<institution><![CDATA[,Instituto Nacional de Saúde Dr. Ricardo Jorge Observatório Nacional de Saúde ]]></institution>
<addr-line><![CDATA[Lisboa ]]></addr-line>
<country>Portugal</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>11</month>
<year>2006</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>11</month>
<year>2006</year>
</pub-date>
<volume>13</volume>
<numero>6</numero>
<fpage>258</fpage>
<lpage>266</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_arttext&amp;pid=S0872-81782006000600001&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_abstract&amp;pid=S0872-81782006000600001&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_pdf&amp;pid=S0872-81782006000600001&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="pt"><p><![CDATA[Estudo do potencial dos genes sabA e hopZ como marcadores de virulência para a doença ulcerosa péptica (DUP) em estirpes de H. pylori de doentes portugueses, 106 isoladas de adultos (50 com DUP, 56 com dispepsia não ulcerosa - DNU) e 74 isoladas de crianças (21 com DUP, 53 com DNU), por PCR e sequenciação. O genótipo sabA on relacionou-se significativamente com a DNU em estirpes isoladas de crianças, enquanto que o genótipo hopZ on foi o mais prevalente em estirpes isoladas de doentes com DUP. Também se verificou a associação significativa entre o genótipo sabA on e os genótipos cagA-, vacAs2 e oipA off, nas estirpes isoladas de crianças, não tendo havido qualquer associação entre a funcionalidade de sabA e hopZ com outros genes, na população adulta. A análise de combinações de genótipos mostrou que, nas estirpes de crianças, o risco para a DUP aumentou quando se associou o genótipo sabA off aos genótipos cagA+, vacAs1 e cagA+/vacAs1. Concluiu-se que os genes sabA e HopZ não constituem marcadores de virulência para DUP numa população Portuguesa. No entanto, sabA off pode contribuir para a distinção entre a DUP e a DNU, quando associado a outros marcadores de virulência.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[To study the potential of sabA and hopZ genes as virulence markers for peptic ulcer disease (PUD) in H. pylori strains isolated from Portuguese patients, 106 isolated from adults (50 with PUD, 56 with non-ulcer dyspepsia) and 74 from children (21 with PUD, 53 with non-ulcer dyspepsia). Genotyping was performed by PCR and sequencing of the 5’ region of the genes was done. We observed that sabA on was significantly more often associated with gastritis only in strains isolated from children. hopZ on was more prevalent in strains from PUD, although this difference was not significant. We also found that sabA on was significantly associated with cagA, vacAs2 and oipA off genotypes in the strains isolated from children and that there was no association between any functional status of sabA and hopZ with other genes in the adult population. Finally, we compared some genotype combinations. In strains isolated from children, the risk for PUD increased when sabA off was associated with: cagA+, vacAs1 and cagA+/vacAs1. We concluded that neither sabA nor hopZ are pathogenicity markers for PUD in this Portuguese population. However, the sabA off genotype can contribute to the distinction between PUD and gastritis when associated with other virulence genes.]]></p></abstract>
</article-meta>
</front><body><![CDATA[ <p><b>Avalia&ccedil;&atilde;o do potencial patog&eacute;nico dos genes <i>sab</i>A e <i>hop</i>Z    de estirpes de Helicobacter Pylori isoladas numa popula&ccedil;&atilde;o portuguesa</b></p>      <p><b>&nbsp;</b><a name="top1"></a>A. Carvalho<sup><a href="#1">1</a></sup>, M.    Oleastro<sup><a href="#1">1</a></sup>, B. Nunes<sup><a href="#2">2</a><a name="top2"></a></sup>,    L. Monteiro</p>      <p>&nbsp;</p>      <p>&nbsp;</p>       <p class=MsoNormal align=center style='text-align:center'><b>Resumo</b><b>&nbsp;</b></p>      <p align="justify">Estudo do potencial dos genes <i>sab</i>A e <i>hop</i>Z como    marcadores de virulência para a doença ulcerosa péptica (DUP) em estirpes de    <i>H. pylori </i>de doentes portugueses, 106 isoladas de adultos (50 com DUP,    56 com dispepsia não ulcerosa - DNU) e 74 isoladas de crianças (21 com DUP,    53 com DNU), por PCR e sequenciação.</p>     <p align="justify">O genótipo <i>sab</i>A <i>on</i><i> </i>relacionou-se significativamente    com a DNU em estirpes isoladas de crianças, enquanto que o genótipo <i>hop</i>Z    <i>on</i><i> </i>foi o mais prevalente em estirpes isoladas de doentes com DUP.    Também se verificou a associação significativa entre o genótipo <i>sab</i>A    <i>on</i><i> </i>e os genótipos <i>cag</i>A-, <i>vac</i>As2 e <i>oip</i>A <i>off</i>,    nas estirpes isoladas de crianças, não tendo havido qualquer associação entre    a funcionalidade de <i>sab</i>A e <i>hop</i>Z com outros genes, na população    adulta. A análise de combinações de genótipos mostrou que, nas estirpes de crianças,    o risco para a DUP aumentou quando se associou o genótipo <i>sab</i>A <i>off</i><i>    </i>aos genótipos <i>cag</i>A+, <i>vac</i>As1 e <i>cag</i>A+/<i>vac</i>As1.</p>     <p align="justify">Concluiu-se que os genes <i>sab</i>A e <i>Hop</i>Z não constituem    marcadores de virulência para DUP numa população Portuguesa. No entanto, <i>sab</i>A    <i>off</i><i> </i>pode contribuir para a distinção entre a DUP e a DNU, quando    associado a outros marcadores de virulência.</p>      <p>&nbsp;</p>      <p class=MsoNormal align=center style='text-align:center'><b>Summary</b></p>      ]]></body>
<body><![CDATA[<p align="justify">To study the potential of sabA and hopZ genes as virulence    markers for peptic ulcer disease (PUD) in H. pylori strains isolated from Portuguese    patients, 106 isolated from adults (50 with PUD, 56 with non-ulcer dyspepsia)    and 74 from children (21 with PUD, 53 with non-ulcer dyspepsia). Genotyping    was performed by PCR and sequencing of the 5&#8217; region of the genes was    done.</p>     <p align="justify">We observed that sabA on was significantly more often associated    with gastritis only in strains isolated from children. hopZ on was more prevalent    in strains from PUD, although this difference was not significant. We also found    that sabA on was significantly associated with cagA, vacAs2 and oipA off genotypes    in the strains isolated from children and that there was no association between    any functional status of sabA and hopZ with other genes in the adult population.    Finally, we compared some genotype combinations. In strains isolated from children,    the risk for PUD increased when sabA off was associated with: cagA+, vacAs1    and cagA+/vacAs1.</p>     <p align="justify">We concluded that neither sabA nor hopZ are pathogenicity markers    for PUD in this Portuguese population. However, the sabA off genotype can contribute    to the distinction between PUD and gastritis when associated with other virulence    genes.</p>     <p align="justify">&nbsp;</p>     <p align="justify">Texto Completo disponível apenas em PDF</p>     <p align="justify">Full text only available in PDF format</p>     <p align="justify">&nbsp;</p>     <p align="justify">&nbsp;</p>      <p class=MsoNormal align=center style='text-align:center'><b>Bibliografia</b><b></b></p>     <p>&nbsp;</p>      ]]></body>
<body><![CDATA[<!-- ref --><p align="justify">1. Cover T. L., D. E. Berg, M. J. Blaser and H. L. T. Mobley.    <i>Helicobacter pylori </i>pathogenesis, p. 509-558. In E. Groisman (ed), Principles    of bacterial pathogenesis, 2001, Academic Press, New York, N.Y.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;[&#160;<a href="javascript:void(0);" onclick="javascript: window.open('/scielo.php?script=sci_nlinks&ref=000023&pid=S0872-8178200600060000100001&lng=','','width=640,height=500,resizable=yes,scrollbars=1,menubar=yes,');">Links</a>&#160;]<!-- end-ref --><p align="justify">2. Dunn, B. E., H. Cohen and M. J. Blaser. <i>Helicobacter    pylori</i>. Clin Microbiol, 1997, Rev. 10: 720-741.</p>     <p align="justify">3. Levinson G. and G. A. Gutman. Slipped-strand Mispairing:    a major mechanism for DNA sequence evolution. Mol. Biol. Evol, 1987, 4: 203-221.</p>     <p align="justify">4. Henderson I., P. Owen, and J. Nataro. Molecular switches    &#8211; the ON and OFF of bacterial phase variation. Molecular Microbiology,    1999; 33; 919-932.</p>     <p align="justify">5. Mahdavi J, B. Sonden, M. Hurtig, F. O. Olfat, L. Forsberg,    N. Roche, et al. <i>Helicobacter pylori </i>sabA adhesin in persistent infection    and chronic inflammation. Science, 2002; 297: 573-8.</p>     <p align="justify">6. Peck B., M. Ortkamp, K. D. Diehl, E. Hundt and B. Knapp.    Conservation, localization and expression of HopZ, a protein involved in adhesion    of <i>Helicobacter pylori</i>, 1999, Nucleic AcidsResearch, vol. 27. no. 16,    3325- 3333.</p>     <p align="justify">7. Galmiche A, J. Rassow, A. Doye, S. Cagnol, J.C. Chambard,    S. Contamin, et al. The N- terminal 34 KDa fragment of <i>Helicobacter pylori    </i>vacuolating cytotoxin targets mithocondria and induces cytochrome c release.    EMBO J 2000; 19:6361-62370.</p>     <p align="justify">8. Godoy A. P., M. L. Ribeiro, Y. H. Benvengo, L Vitiello.,    M. B. Miranda, S. Mendonca, <i>et</i><i> al.</i> Analysis of antimicrobial susceptibility    and virulence factors in <i>Helicobacter pylori </i>clinical isolates, BMC Gastroenterol,    2003; 3: 1-6.</p>     <p align="justify">9. Blaser MJ and Atherton. J. C. <i>Helicobacter pylori </i>persistence:    biology and disease. J Clin Invest, 2004. 113:321-33.</p>     <p align="justify">10. Akopyants N. S., Clifton S. W., Kersulyte, Crabtree J.    E., Youree B. E., Reece C. A., <i>et al</i>. Analyses of the cag pathogenicity    island of <i>Helicobacter pylori</i>. Molecular Microbiology, 1998, 28 (1),    37:53.</p>     ]]></body>
<body><![CDATA[<p align="justify">11. Stein M., R. Rappuoli, and A. Covacci. Tyrosine phosphorylation    of the Helicobacter pylori CagA antigen after cag-driven host cell translocation.    Proc Natl Acad Sci USA, 2000, 97-1263:1268.</p>     <p align="justify">12. Alm R. A., L. S. Ling, D. T. Moir, B. L. King, E. D. Brown,    P. C. Doig, <i>et al</i>. Genomic sequence comparison of two unrelated isolates    of the human gastric pathogen <i>Helicobacter pylori</i>. Nature. 1999, 397:    176-180.</p>     <p align="justify">13. Tomb J.F., O. White, A. R. Kerlavage, R. A. Clayton, G.    G. Sutton, R. D. Fleischmann, <i>et al</i>. The complete genome of the gastric    pathogen <i>Helicobacter pylori</i>. Nature, 1997, 388: 539-547.</p>     <p align="justify">14. Oleastro M, M. Gerhard, A. I. Lopes, P. Ramalho, J. Cabral,    A. S. Guerreiro, et al. <i>Helicobacter pylori </i>virulence genotypes in Portuguese    children and adults with gastroduodenal pathology. Eur J Clin Microbiol Infect    Dis, 2003, 22:85-91.</p>     <p align="justify">15. Lehours P., A. Ménard, S. Dupouy, B. Bergey, F. Richy,    F. Zerbib, <i>et al</i>. Evaluation of the Association of Nine <i>Helicobacter    pylori </i>Virulence Factors with Strains Involved in Low-Grade Gastric Mucosa    - Associated Lymphoid Tissue Lymphoma. Infect. Immun, 2004, 880-888.</p>     <p align="justify">16. de Jonge R., R. G. J. Pot, R. J. L. F. Loffeld, A. H. M    van Vliet., E. J. Kuipers, J. G. Kusters. The functional status of the <i>Helicobacter    pylori sabB</i> adhesin gene as a putative marker for disease outcome. Helicobacter,    2004, 9: 158-64.</p>     <p align="justify">17. J. L. Guruge, P. G. Falk, R. G. Lorenz, M. Dans, H. P.    Wirth, M. J. Blaser, <i>et al</i>. Epithelial attachment alters the outcome    of <i>Helicobacter pylori </i>infection. Proc. Natl. Acad. Sci. USA. 1998, vol.    95, 3925: 3930.</p>     <p align="justify">18. Blom J., A. Gernow, S. Holck, V. Wewer, A. Norgaard, L.    B. Graff, et al. Different patterns of <i>Helicobacter pylori </i>adherence    to gastric mucosa cells in children and adults. An ultrastructural study. Scand    J Gastroenterol. 2000, 35 (10) - 1033: 40.</p>     <p align="justify">19. Sipponen P, Lindgren J. Sialylated Lewis determinant CA    19-9 in benign and malignant gastric tissue. Acta Pathol Microbiol Immunol Scand    [A]. 1986 Sep; 94(5): 305-11.</p>     <p align="justify">20. Amado M, Carneiro F, Seixas M, Clausen H, Sobrinho-Simoes    M. Dimeric sialyl-Le(x) expression in gastric carcinoma correlates with venousinvasion    and poor outcome. Gastroenterology. 1998 Mar; 114(3): 462-70.</p>      ]]></body>
<body><![CDATA[<p>&nbsp;</p>     <p>Correspondência:</p>     <p>L. Monteiro</p>     <p>Centro de Bacteriologia.</p>     <p>Instituto Nacional de Saúde Dr. Ricardo Jorge</p>     <p>Av. Padre Cruz, 1649-016 Lisboa, Portugal</p>     <p>Tel.: +351-21-7519231</p>     <p>Fax: +351-21-7526400</p>     <p><i>e-mail: </i><a href="mailto:m.lurdes.monteiro@insa.min-saude.pt">m.lurdes.monteiro@insa.min-saude.pt</a></p>     <p>&nbsp;</p>     ]]></body>
<body><![CDATA[<p><a name="1"></a>(<a href="#top1">1</a>) Unidade de Helicobacter/Campylobacter/    Centro de Bacteriologia, Instituto Nacional de Saúde Dr. Ricardo Jorge. Lisboa,    Portugal.</p>      <p><a name="2"></a>(<a href="#top2">2</a>) Observatório Nacional de Saúde, Instituto    Nacional de Saúde Dr. Ricardo Jorge. Lisboa, Portugal.</p>     <p>&nbsp;</p>     <p align="right">Recebido para publicação: 11/11/2005</p>     <p align="right">Aceite para publicação: 23/06/2006</p>      <p>&nbsp;</p>  </div>       ]]></body><back>
<ref-list>
<ref id="B1">
<nlm-citation citation-type="">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Cover]]></surname>
<given-names><![CDATA[T. L.]]></given-names>
</name>
<name>
<surname><![CDATA[Berg]]></surname>
<given-names><![CDATA[D. E.]]></given-names>
</name>
<name>
<surname><![CDATA[Blaser]]></surname>
<given-names><![CDATA[M. J.]]></given-names>
</name>
<name>
<surname><![CDATA[Mobley]]></surname>
<given-names><![CDATA[H. L. T.]]></given-names>
</name>
</person-group>
<article-title xml:lang="en"><![CDATA[Helicobacter pylori pathogenesis]]></article-title>
<person-group person-group-type="editor">
<name>
<surname><![CDATA[Groisman]]></surname>
<given-names><![CDATA[E.]]></given-names>
</name>
</person-group>
<source><![CDATA[Principles of bacterial pathogenesis]]></source>
<year>2001</year>
<edition>Academic Press</edition>
<page-range>509-558</page-range><publisher-loc><![CDATA[New York ]]></publisher-loc>
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</back>
</article>
