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:748-1</font></em></font></strong></font></td></tr><tr><td colspan=2><br><br><table align=center width=700><tr><td>Área: <b>Imunologia ( Divisão E )</b><p align=justify><strong>COMENSAL MICROBIOTA-INDUCED ANTIBODIES ARE ESSENTIAL FOR THE HOST TO MOUNT ACUTE INFLAMMATORY RESPONSES.<BR><DIV STYLE="TEXT-ALIGN: LEFT;"> </DIV></strong></p><p align=justify><b><u>Caio Tavares Fagundes </u></b> (<i>UFMG</i>); <b>Angélica Thomaz Vieira </b> (<i>UFMG</i>); <b>Flávio Almeida Amaral </b> (<i>UFMG</i>); <b>Daniel Cisalpino </b> (<i>UFMG</i>); <b>Leda Quércia Vieira </b> (<i>UFMG</i>); <b>Jacques Nicoli </b> (<i>UFMG</i>); <b>Lirlândia Pires de Sousa </b> (<i>UFMG</i>); <b>Mauro Martins Teixeira </b> (<i>UFMG</i>); <b>Danielle da Glória de Souza </b> (<i>UFMG</i>)<br><br></p><b><font size=2>Resumo</font></b><p align=justify class=tres><font size=2><span style="font-family: Arial,Helvetica,sans-serif;">Introduction: Germ free (GF) mice are hyporresponsive to inflammatory challenges, such as ischemia-reperfusion injury (IR) or pulmonary bacterial infection. This is due to enhanced IL-10 production after stimulation, which dampens synthesis of pro-inflammatory mediators. Of note, GF mice present altered antibodies profiles and titers. Then, we intended to check if this different antibodies profile accounts for GF inflammatory hyporresponsiveness. Methods: For antibody reposition, GF mice recieved 400 </span><span style="font-family: Symbol;"><span style="font-family: Arial,Helvetica,sans-serif;"><span style="font-family: Symbol;">m</span><span style="font-family: Arial,Helvetica,sans-serif;">L of inactivated serum (56oC, 60 min) obtained from conventional (CV) mice, GF mice, Immunoglobulin-deficient (MuT) mice, or conventionalized GF (CGF) mice. For conventionalization of GF mice, animals received a suspension of feces (10% in PBS, 200 <span style="font-family: Symbol;">m</span>L, orally) obtained from CV, 14 days before serum collection. 24 hours after serum administration, mice were submmited to intestinal IR. Inflammatory response in the intestine was monitored by neutrophil recruitiment (assessment by Myeloperoxidase activity quantification), vascular permeability measurement (by Evans Blue dye concentration), and quantification of TNF-<span style="font-family: Symbol;">a</span>, CXCL2 and IL-10 levels (by ELISA). Results and conclusion: GF mice that received serum of GF mice did not present alteration in the inflammatory parameters after IR. These animals produced elevated levels of IL-10 in the reperfused tissue, when compared with CV mice submitted to IR. CV-mice serum to GF mice reversed this pattern, leading to reduction in IL-10 production and to elevation in TNF-<span style="font-family: Symbol;">a</span> and CXCL2 synthesis, neutrophil influx and tissue injury after IR. However, MuT mice serum administration was not able to restore GF ability to respond to IR. Hence, these animals presented reduced tissue injury, diminished production of pro-inflammatory cytokines, and elevated IL-10 production after IR, suggesting that antibodies present in serum are necessary to the effects observed after CV serum administration to GF mice. Finally, similarly to CV-serum-treated GF mice, CGF serum-treated mice presented elevated TNF-<span style="font-family: Symbol;">a</span> and CXCL2 production, neutrophil influx and tissue injury after IR. These alterations occurred in parallel to reduction in IL-10 levels in the intestine. Then, we conclude that the idigenous microbiota shapes host ability to respond to inflammatory stimuli through promotion of antibodies production. Support: CNPq, FAPEMIG</span><br><br></span></span> </font></p><br><b>Palavras-chave: </b>&nbsp;microbiota comensal, inflamação, IL-10, isquemia e reperfusão</td></tr></table></tr></td></table></body></html>