The etiology of IBD is unknown. Several factors may be involved, such as GI lymphoid tissue (GALT); permeability defects; genetic, ischemic, biochemical, and psychosomatic disorders; infectious and parasitic agents; dietary allergens; and adverse drug reactions. IBD may also be immune mediated. The intestinal mucosa has a barrier function and controls exposure of antigens to GALT. The latter can stimulate protective immune responses against pathogens, while remaining tolerant of harmless environmental antigens (eg, commensal bacteria, food). Defective immunoregulation of GALT results in exposure and adverse reaction to antigens that normally would not evoke such a response. Although dietary allergy is an unlikely cause of IBD (except in eosinophilic gastroenteritis), it may contribute to increased mucosal permeability and food sensitivity.
Current evidence supports the likely involvement of hypersensitivity reactions to antigens (eg, food, bacteria, mucus, epithelial cells) in the intestinal lumen or mucosa. More than one type of hypersensitivity reaction is involved in IBD. For example, type I hypersensitivity is involved in eosinophilic gastroenteritis, whereas type IV hypersensitivity is likely involved in granulomatous enteritis. The hypersensitivity reaction incites the involvement of inflammatory cells, resulting in mucosal inflammation that impairs the mucosal barrier, in turn facilitating increased intestinal permeability to additional antigens. Persistent inflammation may result in fibrosis.