Inflammatory bowel disease is associated with changes of enterocytic junctions

American Journal of Physiology - Gastrointestinal and Liver Physiology - Tập 281 Số 1 - Trang G216-G228 - 2001
Nikolaus Gaßler1, Claudia M. Rohr1, Armin Schneider2, Jürgen Kartenbeck3, A. Bach2, Nicholas Obermüller4,5, Herwart F. Otto1, Frank Autschbach1
1Pathologisches Institut, Universität Heidelberg, 69120 Heidelberg;
2BASF-LYNX Bioscience AG, 69120 Heidelberg;
3Deutsches Krebsforschungszentrum, 69120, Heidelberg
4Universität Frankfurt, Abteilung Nephrologie, IV. Medizinische Klinik, 60590 Frankfurt, Germany
5Universität Heidelberg, ZMF, Klinikum Mannheim, 68167 Mannheim; and

Tóm tắt

Changes of the intestinal mucosal barrier are considered to play a role in the pathogenesis of inflammatory bowel disease (IBD). Our experiments were designed to identify dysregulation of epithelial junctional molecules in the IBD intestinum and to address whether altered expression of these molecules is a primary event in IBD or a phenomenon secondary to the inflammatory process. Noninflamed and inactively and actively inflamed mucosal tissues from patients with ulcerative colitis or Crohn's disease as well as tissues from control subjects were analyzed for the expression of junctional molecules by different methods. Marked downregulation of junctional proteins and their respective mRNAs was observed in actively inflamed IBD tissues. In IBD tissues with inactive inflammation, only a few junctional molecules such as E-cadherin and α-catenin were affected, whereas expression of desmosomal or tight junction-associated proteins appeared almost unchanged. In noninflamed IBD tissues, junctional protein expression was not different from that seen in normal control subjects. In IBD, downregulation of junctional molecule expression is apparently associated with the inflammatory process and does not likely represent a primary phenomenon.

Từ khóa


Tài liệu tham khảo

10.1083/jcb.133.1.43

10.1016/S0016-5085(97)70180-X

10.1007/BF00996219

10.1006/bbrc.1995.2015

10.1016/0003-9861(89)90532-8

Chomcyznski P., 1993, Biotechniques, 15, 532

10.1136/jcp.48.2.143

Fries W, 1999, Lab Invest, 79, 49

10.1083/jcb.141.7.1539

10.1136/gut.36.6.857

10.1136/gut.29.4.516

10.1073/pnas.93.20.10779

Hanby AM, 1996, Am J Pathol, 148, 723

10.1126/science.270.5239.1203

10.1053/gast.1996.v110.pm8613043

10.1083/jcb.138.1.181

10.1016/S0079-6603(08)60281-0

Jankowski JAZ, 1998, Lab Invest, 78, 1155

10.1002/(SICI)1096-9896(199808)185:4<413::AID-PATH125>3.0.CO;2-K

10.1016/S0016-5085(00)70351-9

Koch PJ, 1991, Eur J Cell Biol, 55, 200

10.1016/S0074-7696(08)60153-9

10.1038/227680a0

10.3181/00379727-214-44099

Marin ML, 1983, Am J Gastroenterol, 9, 537

10.1083/jcb.142.1.117

10.1136/gut.44.2.283

10.1146/annurev.physiol.60.1.121

10.1152/ajpgi.2000.279.2.G250

10.1002/(SICI)1521-1878(199912)22:1<1021::AID-BIES6>3.0.CO;2-P

10.1136/gut.35.1.68

10.1006/geno.1996.0136

North AJ, 1999, J Cell Sci, 112, 4325, 10.1242/jcs.112.23.4325

10.1007/BF02090367

10.1007/BF01540405

10.1016/S0950-3528(96)90045-7

10.1083/jcb.132.3.451

Schmidt A, 1994, Eur J Cell Biol, 65, 229

10.1016/S0016-5085(99)70126-5

10.1136/gut.44.1.96

10.1016/S0016-5085(99)70551-2

10.1093/nar/15.23.10058

10.1146/annurev.cellbio.14.1.89

10.1016/0955-0674(92)90101-H

10.1136/bmj.1.4979.1315

10.1210/endo.137.11.8895364

10.2144/97221pf02

10.1016/0140-6736(93)90882-H

10.1152/ajpgi.1999.276.5.G1279

Thông tin
Thông tin xuất bản

American Journal of Physiology - Gastrointestinal and Liver Physiology

Tập 281 Số 1

G216-G228

Thông tin tác giả