ÿþ<HTML><HEAD><TITLE>25º Congresso Brasileiro de Microbiologia </TITLE><link rel=STYLESHEET type=text/css href=css.css></HEAD><BODY aLink=#ff0000 bgColor=#FFFFFF leftMargin=0 link=#000000 text=#000000 topMargin=0 vLink=#000000 marginheight=0 marginwidth=0><table align=center width=700 cellpadding=0 cellspacing=0><tr><td align=left bgcolor=#cccccc valign=top width=550><font face=arial size=2><strong><font face=Verdana, Arial, Helvetica, sans-serif size=3><font size=1>25º Congresso Brasileiro de Microbiologia </font></font></strong><font face=Verdana size=1><b><br></b></font><font face=Verdana, Arial,Helvetica, sans-serif size=1><strong> </strong></font></font></td><td align=right bgcolor=#cccccc valign=top width=150><font face=arial size=2><strong><font face=Verdana, Arial, Helvetica, sans-serif size=1><font size=1>ResumoID:1678-2</font></em></font></strong></font></td></tr><tr><td colspan=2><br><br><table align=center width=700><tr><td>Área: <b>Patogenicidade Microbiana ( Divisão D )</b><p align=justify><strong> <FONT SIZE="4"><SPAN STYLE="FONT-STYLE: ITALIC;">BABA</SPAN>2 AS A RISK FACTOR FOR DUODENAL ULCER IN CHILDHOOD </FONT> </strong></p><p align=justify><b>Gifone Aguiar Rocha </b> (<i>F. Medicina/UFMG</i>); <b><u>Sergio de Assis Batista </u></b> (<i>ICB-UFMG</i>); <b>Juliana Pinto Silva </b> (<i>ICB-UFMG</i>); <b>Andreia Maria Camargos Rocha </b> (<i>F. Medicina/UFMG</i>); <b>Paulo Bittencourt </b> (<i>HC-UFMG</i>); <b>Mônica Maria Demas Álvares Cabral </b> (<i>F. Medicina/UFMG</i>); <b>Dulciene Maria de Magalhães Queiroz </b> (<i>F. Medicina/UFMG</i>)<br><br></p><b><font size=2>Resumo</font></b><p align=justify class=tres><font size=2> <p class="MsoNormal" style="text-align: justify;"><font size="4"><i style="font-family: Arial,Helvetica,sans-serif;"><span style="" lang="EN-US">Helicobacter pylori</span></i><span style="font-family: Arial,Helvetica,sans-serif;" lang="EN-US"> infection is acquired predominantly in childhood and persists lifelong. The infection may progress to different clinical outcomes as different as duodenal ulcer and gastric carcinoma. Although the factors that determine the outcome of the infection are not well understood, bacterial virulence factors have been suggested to play important roles. One of the major viulence factors of <i style="">H. pylori</i> is the cytotoxin vaculating cytotoxin (VacA), which causes cytoplasmic vacuolation in gastric epithelial cells. Another well characterized virulence factor is the cytotoxin-associatyed antigen (CagA), which is encoded by a one of the genes located in the <i style="">cag</i> pathogenicity island. </span></font><span style="" lang="EN"><font size="4"><span style="font-family: Arial,Helvetica,sans-serif;">The blood group antigen binding adhesin BabA encoded by the </span><i style="font-family: Arial,Helvetica,sans-serif;">babA</i><span style="font-family: Arial,Helvetica,sans-serif;">2 gene, mediates the adherence of </span><i style="font-family: Arial,Helvetica,sans-serif;">H. pylori</i><span style="font-family: Arial,Helvetica,sans-serif;"> to human Lewis B blood group antigen on gastric epithelial cells. The attachment may facilitate </span><i style="font-family: Arial,Helvetica,sans-serif;">H. pylori</i><span style="font-family: Arial,Helvetica,sans-serif;"> colonization and efficient delivery of virulence factors such as VacA and CagA to the host cells, resulting in severe gastric inflammation. In Western populations, the </span><i style="font-family: Arial,Helvetica,sans-serif;">babA</i><span style="font-family: Arial,Helvetica,sans-serif;">2 gene has been associated with peptic ulcer and gastric carcinoma. However, there are no studies evaluating </span><i style="font-family: Arial,Helvetica,sans-serif;">bab</i><i style="font-family: Arial,Helvetica,sans-serif;">A</i><span style="font-family: Arial,Helvetica,sans-serif;">2 virulent marker in children with duodenal ulcer. Therefore, we investigated the presence of </span><i style="font-family: Arial,Helvetica,sans-serif;">babA</i><span style="font-family: Arial,Helvetica,sans-serif;">2, by PCR, using the primer set described by Gerhard </span><i style="font-family: Arial,Helvetica,sans-serif;">et</i><span style="font-family: Arial,Helvetica,sans-serif;"> </span><i style="font-family: Arial,Helvetica,sans-serif;">al</i><span style="font-family: Arial,Helvetica,sans-serif;">, in 137 children (37 with duodenal ucler, 64 boys, mean age 10.28 ± 3.75 yr; range 1-18 yr). Since the results were ambiguous, we sequenced a DNA fragment containing the primer annealing sites and the signal sequence of the gene of all strains. </span><i style="font-family: Arial,Helvetica,sans-serif;">cag</i><i style="font-family: Arial,Helvetica,sans-serif;">A</i><span style="font-family: Arial,Helvetica,sans-serif;"> status was evaluated by PCR using two sets of primers. Gastritis was classified according to the revised </span><st1:place style="font-family: Arial,Helvetica,sans-serif;" w:st="on"><st1:city w:st="on">Sydney</st1:city></st1:place><span style="font-family: Arial,Helvetica,sans-serif;"> system. Data were analyzed by logistic models, adjusting for confounding factors. </span><i style="font-family: Arial,Helvetica,sans-serif;">bab</i><i style="font-family: Arial,Helvetica,sans-serif;">A</i><span style="font-family: Arial,Helvetica,sans-serif;">2 was present in all </span><i style="font-family: Arial,Helvetica,sans-serif;">H. pylori</i><span style="font-family: Arial,Helvetica,sans-serif;"> strains, but nucleotide deletions (121 - 88.3%) and a nucleotide substitution C&#8594;T 114 (83.2%) were observed in the upstream region near to the gene signal sequence. The nucleotide substitution was associated with the nucleotide deletions (p&lt;10</span><sup style="font-family: Arial,Helvetica,sans-serif;">-3</sup><span style="font-family: Arial,Helvetica,sans-serif;">). The nucleotide substitution was negatively associated with the degree of polymorphonuclear neutrophil cells (p=0.04), the presence of lymphoid follicles (p = 0.05) and erosion (p = 0.001) in the corpus mucosa, suggesting a functional mutation. In the multivariate analyses, </span><i style="font-family: Arial,Helvetica,sans-serif;">cag</i><i style="font-family: Arial,Helvetica,sans-serif;">A</i><span style="font-family: Arial,Helvetica,sans-serif;"> status (OR = 4.4, 95%C I= 1.6 - 12.2), male gender (OR = 4.1, 95%CI = 1.6 - 10.2) and age (OR=1.2, 95%CI=1.1-1.4) were independently associated with duodenal ulcer, but the </span><i style="font-family: Arial,Helvetica,sans-serif;">bab</i><i style="font-family: Arial,Helvetica,sans-serif;">A</i><span style="font-family: Arial,Helvetica,sans-serif;">2 variations were not. Grants/ FAPEMIG/CNPq.</span></font> <span style="color: black;"><o:p></o:p></span></span></p> </font></p><br><b>Palavras-chave: </b>&nbsp;Helicobacter pylori, BabA, duodenal ulcer</td></tr></table></tr></td></table></body></html>