Inflammatory bowel disease (IBD), which encompasses both Crohn's disease and ulcerative colitis, is a chronically relapsing intestinal disorder that is characterized by diarrhea and abdominal pain. The incidence of IBD is increasing worldwide. Although some major advances have been made in recent years, the pathogenesis of the disease still remains obscure. As currently understood, a combination of genetic alterations and immunological disturbances causing an interaction of the enteric microflora with the underlying mucosa and a disrupted barrier function may be crucial for the development of disease. Despite substantial new data that have been obtained over the last several years, it has become increasingly difficult to accommodate these into a unifying disease model. Identification of pro- and anti-inflammatory cytokines has introduced "biologic therapies," but treatment of IBD is still based mainly on broad-spectrum immunosuppressive drugs such as steroids and azathioprine. In this volume, the most relevant pathogenetic aspects are stressed: genetic alterations, disrupted epithelial barrier function, immunological disturbances, and the role of the enteric microflora. NOTE: Annals volumes are available for sale as individual books or as a journal. For information on institutional journal subscriptions, please visit www.blackwellpublishing.com/nyas.ACADEMY MEMBERS: Please contact the New York Academy of Sciences directly to place your order (www.nyas.org). Members of the New York Academy of Science receive full-text access to the Annals online and discounts on print volumes. Please visit http://www.nyas.org/MemberCenter/Join.aspx for more information about becoming a member.

Inflammatory bowel disease (IBD), which encompasses both Crohn's disease and ulcerative colitis, is a chronically relapsing intestinal disorder that is characterized by diarrhea and abdominal pain. The incidence of IBD is increasing worldwide. Although some major advances have been made in recent years, the pathogenesis of the disease still remains obscure. As currently understood, a combination of genetic alterations and immunological disturbances causing an interaction of the enteric microflora with the underlying mucosa and a disrupted barrier function may be crucial for the development of disease. Despite substantial new data that have been obtained over the last several years, it has become increasingly difficult to accommodate these into a unifying disease model. Identification of pro- and anti-inflammatory cytokines has introduced "biologic therapies," but treatment of IBD is still based mainly on broad-spectrum immunosuppressive drugs such as steroids and azathioprine. In this volume, the most relevant pathogenetic aspects are stressed: genetic alterations, disrupted epithelial barrier function, immunological disturbances, and the role of the enteric microflora. NOTE: Annals volumes are available for sale as individual books or as a journal. For information on institutional journal subscriptions, please visit www.blackwellpublishing.com/nyas.ACADEMY MEMBERS: Please contact the New York Academy of Sciences directly to place your order (www.nyas.org). Members of the New York Academy of Science receive full-text access to the Annals online and discounts on print volumes. Please visit http://www.nyas.org/MemberCenter/Join.aspx for more information about becoming a member.