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:749-1</font></em></font></strong></font></td></tr><tr><td colspan=2><br><br><table align=center width=700><tr><td>Área: <b>Virologia ( Divisão P )</b><p align=justify><strong>
<SPAN STYLE="FONT-FAMILY: TIMES NEW ROMAN,TIMES,SERIF;">TBXA2 PLAYS AN IMPORTANT ROLE IN THE VASCULAR AND INFLAMMATORY ALTERATIONS INDUCED BY DV INFECTION.</SPAN>    
</strong></p><p align=justify><b><u>Daniel Cisalpino </u></b>  (<i>UFMG</i>); <b>Caio  Fagundes </b>  (<i>UFMG</i>); <b>Rodrigo  Guabiraba </b>  (<i>UFMG</i>); <b>Flávio  Amaral </b>  (<i>UFMG</i>); <b>Rafael  Souza </b>  (<i>UFMG</i>); <b>Lirlândia  Sousa </b>  (<i>UFMG</i>); <b>Mauro  Teixeira </b>  (<i>UFMG</i>); <b>Danielle  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="" lang="EN-US"><span style="font-weight: bold;">Introduction:</span> Dengue virus (DV) has emerged as  the most relevant arthropod-borne virus in tropical areas. During the infection,  it is observed increase in the vascular permeability, haemoconcentration and  thrombocytopenia. Eicosanoids are a major class of lipid mediators involved in  several homeostatic and inflammatory processes. Our group is evaluating the  importance of Thromboxane A<sub>2</sub> (TBXA<sub>2</sub>) and its receptors in an experimental model  of Dengue virus serotype 2 (DEN-2) infection. <span style="font-weight: bold;">Methods:</span> <span style="text-transform: uppercase;">Balb</span>/c mice were infected intra-peritoneally with 1 PFU of  DEN-2, and, from the 5<sup>th </sup>day of infection, received the following treatments:  Acetyl Salicylic Acid (AAS) (dose of 100, 10 and 1 mg/kg), BMS 180291 (20mg/kg,  antagonist for Thromboxane receptors) and Indomethacin (INDO) (2mg/kg).  Non-infected mice, and animals treated only with drug vehicle were used as  controls. After infection, lethality rates, hematocrit levels and platelet  number, viral titers, cytokine production and neutrophil influx were evaluated.  <span style="font-weight: bold;">Results and Discussion:</span><b style=""> </b>Treated  animals showed an improved clinical condition as indicated by reduced hematocrit  and higher platelet count. Inflammatory parameters, such as production of cytokines  in the liver, in the spleen and in the lungs and MPO activity in these organs,  were also significantly decreased in the treated groups. The observed effects  were dose dependent for AAS, and the 100mg/kg-treated group presented similar results  to that found in BMS treated animals. This suggests that the reduced  inflammatory response in the treated groups studied were due to blockade of TBXA<sub>2</sub>  action. However, none of the treated groups showed smaller lethality rates that  vehicle-treated ones, probably to high viral loads found after infection. Conclusion:  TBXA<sub>2</sub> plays a significant role in the characteristic inflammatory alterations  induced by DV infection, and its blockade results in reduced inflammatory  response after disease onset. However, TBXA<sub>2</sub> inhibition does not interfere in  host ability to control the infection.<br><br>Financial Support: CNPq, FAPEMIG<br></span>    
</font></p><br><b>Palavras-chave: </b>&nbsp;Dengue, Eicosanoids, Inflammation, Infection, Thromboxane A2</td></tr></table></tr></td></table></body></html>