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Utilizing polarized T-84 cells, an intestinal epithelial cell line derived from colon carcinoma grown on semipermeable tissue culture inserts, we determined that infection with a\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Salmonella enterica<\/jats:named-content>\n                    serovar Typhimurium\n                    <jats:italic>csgBA<\/jats:italic>\n                    mutant, which does not express curli, resulted in an increase in intestinal barrier permeability and an increase in bacterial translocation compared to infection with curliated wild-type\n                    <jats:italic>S<\/jats:italic>\n                    . Typhimurium. When the TLR2 downstream signaling molecule phosphatidylinositol 3-kinase (PI3K) was blocked using wortmannin or LY294002, the difference in disruption of the intestinal epithelium and bacterial translocation was no longer observed. Additionally, disruption of polarized T-84 cells treated basolaterally with the TLR5 ligand flagellin was prevented when the polarized cells were simultaneously treated with the synthetic TLR2\/TLR1 ligand Pam\n                    <jats:sub>3<\/jats:sub>\n                    CSK\n                    <jats:sub>4<\/jats:sub>\n                    or with purified curli fibrils in the apical compartment. Similar to\n                    <jats:italic>in vitro<\/jats:italic>\n                    observations, C57BL\/6 mice infected with the\n                    <jats:italic>csgBA<\/jats:italic>\n                    mutant suffered increased disruption of the intestinal epithelium and therefore greater dissemination of the bacteria to the mesenteric lymph nodes than mice infected with wild-type\n                    <jats:italic>S<\/jats:italic>\n                    . Typhimurium. The differences in disruption of the intestinal epithelium and bacterial dissemination in the mice infected with\n                    <jats:italic>csgBA<\/jats:italic>\n                    mutant or wild-type\n                    <jats:italic>S<\/jats:italic>\n                    . Typhimurium were not apparent in TLR2-deficient mice. Overall, these studies report for the first time that activation of the TLR2\/PI3K pathway by microbial amyloids plays a critical role in regulating the intestinal epithelial barrier as well as monitoring bacterial translocation during infection.\n                  <\/jats:p>","DOI":"10.1128\/iai.00453-12","type":"journal-article","created":{"date-parts":[[2012,12,4]],"date-time":"2012-12-04T08:47:23Z","timestamp":1354610843000},"page":"478-486","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":65,"title":["Epithelial Cells Augment Barrier Function via Activation of the Toll-Like Receptor 2\/Phosphatidylinositol 3-Kinase Pathway upon Recognition of Salmonella enterica Serovar Typhimurium Curli Fibrils in the Gut"],"prefix":"10.1128","volume":"81","author":[{"given":"Gertrude O.","family":"Oppong","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glenn J.","family":"Rapsinski","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiffanny N.","family":"Newman","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessalyn H.","family":"Nishimori","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven G.","family":"Biesecker","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00c7agla","family":"T\u00fckel","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1734063100"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature06244"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1124234"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature08821"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.0040003"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2114"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/77783"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212115200"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.48.2.176"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1127119"},{"key":"e_1_3_2_12_2","first-page":"G993","article-title":"HIP\/PAP is an adhesive protein expressed in hepatocarcinoma, normal Paneth, and pancreatic cells","volume":"271","author":"Christa L","year":"1996","unstructured":"ChristaLCarnotFSimonMTLevavasseurFStinnakreMGLasserreCThepotDClementBDevinoyEBrechotC. 1996. 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