**Meet the editor**

Dr. Imre Laszlo Szabo is a medical doctor holding a Ph. D. degree in Gastroenterology from the University of Pécs (Hungary, 2004), where he studied the mechanisms of cytoprotection and mucosal healing processes in different regions of human gastrointestinal system. He currently works as an Assistant Professor at the First Department of Medicine, University of Pécs and has

10 years of experience in teaching Internal Medicine and Gastroenterology at graduate and postgraduate level. His research in the United States included the study of ulcer healing, nonsteroidal gastroenteropathy in animal models and their molecular mechanisms in isolated cells. He has published his work in several peer reviewed journals and given oral and poster presentations at national and international conferences. In addition he has authored Hungarian grants and participated in grants from U.S. Veteran's Administration. His fields of special expertise include gastrointestinal mucosal injury, defensive and healing mechanisms.

Contents

**Preface VII**

Milan

**Bowel Disease 3**

**and Disease 73**

Chapter 4 **Fibrosis in Crohn's Disease 151**

**Section 2 Management of Disease 175**

**Diseases 197**

Lauri Diehl

and Michael J. Wannemuehler

**and Future Directions 177** Rahul A. Sheth and Michael S. Gee

V. Surlin, C. Copaescu and A. Saftoiu

**Section 1 Pathogenesis of Inflammatory Bowel Disease 1**

Chapter 1 **Insights to the Ethiopathogenesis of the Inflammatory**

Ana Brajdić and Brankica Mijandrušić-Sinčić

Chapter 3 **The Role of the Microbiota in Gastrointestinal Health**

Chapter 2 **Gene Polymorphisms and Inflammatory Bowel Diseases 23**

Chapter 5 **The Imaging of Inflammatory Bowel Disease: Current Concepts**

Chapter 6 **An Update to Surgical Management of Inflammatory Bowel**

Bartosova Ladislava, Kolorz Michal, Wroblova Katerina and Bartos

Anne-Marie C. Overstreet, Amanda E. Ramer-Tait, Albert E. Jergens

## Contents

## **Preface XI**



## **Section 3 Future Therapeutic Directions in IDB 225**

Chapter 7 **Targeting Colon Drug Delivery by Natural Products 227** Hyunjo Kim

#### Chapter 8 **Food Nanoparticles and Intestinal Inflammation: A Real Risk? 259** Alina Martirosyan, Madeleine Polet, Alexandra Bazes, Thérèse

Sergent and Yves-Jacques Schneider

Preface

deposition of collagen.

Inflammatory bowel disease (IBD) is a term for a two very different and yet in many characteristics congruent chronic inflammatory disorder of the intestinal tract. Crohn's disease (CD) and ulcerative colitis are two principal components of IBD. Both CD and ulcerative colitis are considered as multifactoral diseases. For long period of time we keep these inflammatory intestinal disorders as the result of environmental factors and immunological disturbances manifested in persons with genetic predisposition. The pathogenesis of IBD has remained largely unknown, but surely involves environmental factors, immunological factors in a complex form. Increasing disease prevalence and

Epidemiological studies have shown that prevalence of IDB has dramatically increases in western world probably due to western lifestyle. Environmental factors are suggested to have major role in development of diseases connected to westernalization of the lifestyle. These factors include smoking, use of antibiotics and non-steroidal anti-inflammatory drugs, stress, various infections and diet. The initiating mechanisms of their actions are still not understood. Research has revealed several genetic factors contributing to IDB pathogenesis; more than a hundred IDB genes, loci and their allele variation have been

Intestinal stricture is a serious and late complication of CD. Recent studies have identified certain disease specific characteristics that may be used in identifying individuals having higher risk for stricture development. These are lower age at initial diagnosis of CD, need for steroid therapy at the diagnosis, perianal fistulizing disease or small intestinal localized disease. Anti-Saccharomyces cerevisiae antibody (ASCA) levels were also found to be correlated to fibrostenosing or penetrating disease behaviour. Recently, other serological markers (anti-I2 and anti-CBir1), fibronectin, bFGF and YKL-40 glycoprotein of the chitinase family have been shown to lead to the hyperplasia of the intestinal muscle layers and

Determination of gene polymorphism can also be important in regarding the prediction of therapy response. Since no curative therapy for IBD exists, pharmacological therapy mainly focuses on inflammation control. IBD pharmacotherapy utilizes a wide scale of drugs for inflammation reduction including aminosalicylates, glicocorticoids, immunomodulators and biological therapy. Their pharmocodinamics and pharmacokinetics can be altered by polymorphisms of certain gene coding proteins resulting faster drug elimination, tolerance or more side affect development. Namely, the form of N-acetyltransferase in slow acetylators can develop more side effects for sulfasalazine, mutation of glucocorticoid receptor-β lead to decreased affinity to exogenous glucocorticoids, mutations of thiopurine

defined (e.g. NOD2/CARD15, IL23, ATG16L1, IRGM, ICAM-1, CCR5, TLR4, TNFα).

gathered lot of new research data on IBD suggested the pretence for review.
