{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T23:53:01Z","timestamp":1790725981631,"version":"4.1.0"},"reference-count":56,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2006,4,21]],"date-time":"2006-04-21T00:00:00Z","timestamp":1145577600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background:\u2002<\/jats:bold> Inflammatory bowel disease (IBD) affects approximately 4\u2003million people worldwide and can be caused by dysregulated mucosal immune responses to the intestinal commensal microflora. Immunoglobulin A (IgA) is considered to be the principal antibody in intestinal secretions and functions to prevent commensals and pathogenic organisms from gaining access to epithelial cell surfaces. Immunoglobulin A deficiency in humans has been associated with celiac disease and ulcerative colitis. However, the precise role of IgA in the pathogenesis of these disorders is yet to be fully understood.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> Mice with a targeted disruption in IgA production (IgA<jats:sup>\u2013\/\u2013<\/jats:sup> mice) and polymeric immunoglobulin receptor (pIgR<jats:sup>\u2013\/\u2013<\/jats:sup> mice) were analyzed for the contribution of secretory immunity in the pathogenesis of dextran sulfate sodium (2.5%)\u2010induced colitis.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> It was found that dextran sulfate sodium\u2010treated pIgR<jats:sup>\u2013\/\u2013<\/jats:sup> mice displayed greater loss of bodyweight and had severe clinical illness compared to similarly treated IgA<jats:sup>\u2013\/\u2013<\/jats:sup> mice and wild\u2010type animals. Additionally, colonic tissues from the pIgR<jats:sup>\u2013\/\u2013<\/jats:sup> mice exhibited progressively and significantly greater degrees of mucosal edema, ulceration, crypt abscesses and macrophage infiltration when compared to similarly treated IgA<jats:sup>\u2013\/\u2013<\/jats:sup> mice and wild\u2010type animals.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> The results indicate that secretory immunoglobulins contribute to protection of the colonic mucosa against dextran sulfate sodium\u2010induced epithelial injury, although the isotype of the secretory immunoglobulin (IgA or IgM) may not be a decisive factor in such protection. Collectively, the pIgR and\/or the secretory component are important for the maintenance of epithelial integrity and mucosal homeostasis in the colonic epithelium.<\/jats:p>","DOI":"10.1111\/j.1440-1746.2006.04312.x","type":"journal-article","created":{"date-parts":[[2006,4,21]],"date-time":"2006-04-21T20:42:53Z","timestamp":1145652173000},"page":"1372-1380","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Contribution of polymeric immunoglobulin receptor to regulation of intestinal inflammation in dextran sulfate sodium\u2010induced colitis"],"prefix":"10.1111","volume":"21","author":[{"given":"Ashlesh K","family":"Murthy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Candice N","family":"Dubose","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey A","family":"Banas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacqueline J","family":"Coalson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard P","family":"Arulanandam","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,7,28]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1058709"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.micro.51.1.311"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0889-8553(01)00004-8"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra020831"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.288.5474.2222"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-3410-5_11"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.19.8796"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(08)60240-0"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.44.1.2"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-59951-4_6"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0950-3579(96)80003-3"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(03)00122-5"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.15.6901"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1086\/314802"},{"key":"e_1_2_6_16_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.12.040194.000431"},{"key":"e_1_2_6_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(00)00041-5"},{"key":"e_1_2_6_18_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-3083.1994.tb03371.x"},{"key":"e_1_2_6_19_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830191210"},{"key":"e_1_2_6_20_2","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.69.2.289"},{"key":"e_1_2_6_21_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V83.5.1278.1278"},{"key":"e_1_2_6_22_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.1996.d01-793.x"},{"key":"e_1_2_6_23_2","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199408000-00016"},{"key":"e_1_2_6_24_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.42.3.362"},{"key":"e_1_2_6_25_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1081-1206(10)63329-7"},{"key":"e_1_2_6_26_2","doi-asserted-by":"publisher","DOI":"10.3109\/00365529209000089"},{"key":"e_1_2_6_27_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(08)60848-2"},{"key":"e_1_2_6_28_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.38.3.365"},{"key":"e_1_2_6_29_2","doi-asserted-by":"publisher","DOI":"10.1097\/00001574-199511000-00012"},{"key":"e_1_2_6_30_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00917561"},{"key":"e_1_2_6_31_2","doi-asserted-by":"publisher","DOI":"10.1006\/mpat.2001.0477"},{"key":"e_1_2_6_32_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.38.3.348"},{"key":"e_1_2_6_33_2","doi-asserted-by":"crossref","first-page":"2521","DOI":"10.4049\/jimmunol.162.5.2521","article-title":"Targeted deletion of the IgA constant region in mice leads to IgA deficiency with alterations in expression of other Ig isotypes","volume":"162","author":"Harriman GR","year":"1999","journal-title":"J. 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