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| 1 | Intestinal barrier in inflammatory bowel disease显示文摘A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal microorganisms.In this review,we provide an overview about the major components of this protective system as for example an intact epithelium,the synthesis of various antimicrobial peptides(AMPs)and the formation of the mucus layer.We highlight the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease.Barrier disturbances including a defective production of AMPs,alterations in thickness or composition of the intestinal mucus layer,alterations of pattern-recognition receptors,defects in the process of autophagy as well as unresolved endoplasmic reticulum stress result in an inadequate host protection and are thought to play a crucial role in the pathogenesis of the inflammatory bowel diseases Crohn’s disease and ulcerative colitis. | Lena Antoni Sabine Nuding Jan Wehkamp Eduard F Stange | 2014 | World Journal of Gastroenterology2014，20，5： | 33 |
| 2 | From intestinal stem cells to inflammatory bowel diseases显示文摘The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn's disease (CD) and ulcerative colitis (UC), is still complex and under investigation. The importance of the microbial flora in developing IBD is beyond debate. In the last few years, the focus has changed from adaptive towards innate immunity. Crohn's ileitis is associated with a deficiency of the antimicrobial shield, as shown by a reduced expression and secretion of the Paneth cell defensin HD5 and HD6, which is related to a Paneth cell differentiation defect mediated by a diminished expression of the Wnt transcription factor TCF4. In UC, the protective mucus layer, acting as a physical and chemical barrier between the gut epithelium and the luminal microbes, is thin- ner and in part denuded as compared to controls. This could be caused by a missing induction of the goblet cell differentiation factors Hath1 and KLF4 leading to immature goblet cells. This defective Paneth and goblet cell differentiation in Crohn's ileitis and UC may enablethe luminal microbes to invade the mucosa and trigger the inflammation. The exact molecular mechanisms behind ileal CD and also UC must be further clarified, but these observations could give rise to new therapeutic strategies based on a stimulation of the protective innate immune system. | Michael Gersemann Eduard Friedrich Stange Jan Wehkamp | 2011 | World Journal of Gastroenterology2011，17，27： | 19 |
| 3 | Crohn’s disease-Defect in innate defence显示文摘Crohn’s disease may prinicipally involve the whole gastrointestinal tract. Most commonly, the inflammation occurs in the small intestine and/or in the colon with stable disease location over the years. The pathogenesis of both disease phenotypes is complex, the likely primary defect lies in the innate rather than adaptive immunity, particularly in the chemical antimicrobial barrier of the mucosa. Crohn’s ileitis is associated with a reduced expression of the Wnt signalling pathway transcription factor T-cell factor 4 (TCF4), which is regulating Paneth cell differentiation. As a result, the alpha-defensins and principal Paneth cell products HD5 and HD6 are deficiently expressed in ileal disease, independent of current inflammation. In contrast, Crohn’s colitis is typically associated with an impaired induction of the beta-defensins HBD2 and HBD3 caused by fewer gene copy numbers in the gene locus of the beta-defensins on chromosome 8. This ileal and colonic defect in innate defence mediated by a deficiency of the protective alpha- and beta- defensins may enable the luminal microbes to invade the mucosa and trigger the inflammation. A better understanding of the exact molecular mechanisms behind ileal and colonic Crohn’s disease may give rise to new therapeutic strategies based on a stimulation of the protective innate immune system. | Michael Gersemann Jan Wehkamp Klaus Fellermann Eduard Friedrich Stange | 2008 | World Journal of Gastroenterology2008，14，36： | 7 |
| 4 | Intestinal bacterial translocation in rats with cirrhosis is related to compromised paneth cell antimicrobial host defense显示文摘 | Zora Teltschik Reiner Wiest Julia Beisner Sabine Nuding Claudia Hofmann Juergen Schoelmerich Charles L. Bevins Eduard F. Stange Jan Wehkamp | 2012 | Hepatology2012，，： | 2 |
| 5 | Mechanisms of disease:defensins in gastrointestinal disease显示文摘 | WEHKAMP J FELLERMANN K HERRLINGER KR | 2005 | Nat Clin Pract Gastroenterol Hepatol2005，2，： | 1 |
| 6 | Pseudomonas aeruginosa and IL-1 beta-mediated induction of human beta-defensin-2 in keratinocytes is controlled by NF-kappaB and AP-1显示文摘 | Wehkamp K Schwichtenberg L Schroder JM | 2006 | J Invest Dermatol2006，126，1： | 1 |
| 7 | Reduced Paneth cell al-pha-defensins in ileal Crohn's disease显示文摘 | Wehkamp J Salzman NH Porter E | 2005 | Proc Natl Acad Sci U S A2005，102，18： | 1 |
| 8 | Innate immune dysfunction in inflammatory bowel disease显示文摘 | Gersemann M Wehkamp J Stange EF | 2012 | J Intern Med2012，271，5： | 1 |
| 9 | Mechanisms of disease: defensins in gastrointestinal diseases 显示文摘 | Wehkamp J Fellermann K Herrlinger KR | 2005 | Nat Clin Pract Gastroenterol Hepatol2005，2，9： | 1 |
| 10 | Pseudomonas aeruginosa-and IL-1beta-mediated induction of human beta-defensin-2 in keratinocytes is controlled by NF-kappaB and AP-1显示文摘 | WEHKAMP K SCHWICHTENBERG L SCHRODER J M | 2006 | J Invest Dermatol2006，126，： | 1 |
| 11 | Pseudomonas aeruginosa- and IL-lbeta-mediated induction of human beta- defensin-2 in keratinocytes is controlled by NF-kappaB and AP-1 显示文摘 | Wehkamp K Schwichtenberg L Schroder JM | 2006 | J Invest Dermatol2006，126，1： | 1 |
| 12 | Mechanisms of disease:defensins in gastrointestinal diseases 显示文摘 | Wehkamp J Fellermann K Herrlinger KR | 2005 | Nat Clin Pract Gastroenterol Hepatol2005，2，9： | 1 |
| 13 | More than a marine propeller – the flagellum of the probiotic Escherichia coli strain Nissle 1917 is the major adhesin mediating binding to human mucus显示文摘 | Anja Troge Wolfgang Scheppach Bjoern O. Schroeder Stefan A. Rund Klaus Heuner Jan Wehkamp Eduard F. Stange Tobias A. Oelschlaeger | 2012 | International Journal of Medical Microbiology . 2012 (7-8)2012，，7： | 1 |
| 14 | Antimicrobial peptides in the skin 显示文摘 | Fellermann K Wehkamp J Stange EF | 2003 | N Engl J Med2003，348，4： | 1 |
| 15 | Crohn's disease:a defensin deficiency syndrome显示文摘 | Fellermann K Wehkamp J Herrlinger KR | | 0，，06： | 1 |
| 16 | Defensins and other antimicrobial peptides in inflammatory bowel disease 显示文摘 | Wehkamp J Schmid M Stange EF | 2007 | Curr Opin Gastroenterol2007，23，4： | 1 |
| 17 | Crohn's disease:a defensin deficiency syndrome显示文摘 | Klaus Fellermann Jan Wehkamp | 2003 | European J Gastroenterology & Hepatology2003，15，： | 1 |
| 18 | Defensin pattern in chronic gastris: HBD-2 is differentially expressed with respect to Helicobacter pylori status显示文摘 | WEHKAMP J SCHMIDT K HERRLINGER | 2003 | J Clin Pathol2003，56，： | 1 |
| 19 | Paneth's disease 显示文摘 | Wehkamp J Stange EF | 2010 | J Crohns Coli- tis2010，4，： | 1 |
| 20 | Inducible and constitutivel3-defensins are differentially expressed in Crohn' s disease and ulcerative colitis 显示文摘 | Wehkamp J Harder J Weichenthal M | 2003 | Inflamm Bowel Dis2003，9，4： | 1 |
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