Initial events and effector mechanisms of most inflammatory and autoimmune 
diseases remain largely unknown. Dysfunction of the innate and adaptive immune 
systems associated with mucosae (the major interface between the organism and 
its environment, e.g., microbiota, food) can conceivably cause impairment of 
mucosal barrier function and development of localized or systemic inflammatory 
and autoimmune processes. Animal models help in elucidating the etiology and 
pathogenetic mechanisms of human diseases, such as the inflammatory bowel 
diseases, Crohn's disease and ulcerative colitis, severe chronic diseases 
affecting the gut. To study the role of innate immunity and gut microbiota in 
intestinal inflammation, colitis was induced by dextran sulfate sodium (DSS) in 
mice with severe combined immunodeficiency (SCID). Conventionally reared 
(microflora-colonized) SCID mice displayed severe inflammation like that seen in 
immunocompetent Balb/c mice, whereas only minor changes appeared in the 
intestinal mucosa of DSS-fed gnotobiotic germ-free SCID mice. The presence of 
microflora facilitates the inflammation in DSS-induced colitis that develops in 
immunodeficient SCID mice, that is, in the absence of T and B lymphocytes. 
Celiac disease, a chronic autoimmune small bowel disorder, afflicts genetically 
susceptible individuals with wheat gluten intolerance. We showed that, in 
contrast with any other food proteins, wheat gliadin and its peptic fragments 
activate mouse macrophages and human monocytes to produce proinflammatory 
cytokines through the nuclear factor-kappaB signaling pathway. Activation of 
innate immunity cells by food proteins or components from gut microbiota thus 
could participate in the impairment of intestinal mucosa and the development of 
intestinal and/or systemic inflammation.