Dysbiosis crohns disease colita ulceroas intervenia unor bacterii este mai puin documentat. Mecanismul imunologic Exist un deficit primar a sistemului imunitar.
Anomaliile imunitii mediate celular asociate bolilor inflamatorii intestinale sunt : dysbiosis crohns disease cutanat, rspuns redus dysbiosis crohns disease diversi stimuli mitogeni, reducerea numrului de limfocite T periferice  Se consider c aceste boli sunt induse prin anumii factori de mediu pe un teren predispus genetic.
Stresul, depresia pot declansata sau agrava bolile inflamatorii intestinale. Immune Response Both Crohn's disease and ulcerative colitis patients have activated innate macrophage, neutrophil and acquired T and B cell immune responses and loss of tolerance to enteric commensal bacteria Macrophages and dendritic cells in the lamina propria are increased in absolute number and have an activated phenotype in both forms of IBD, but have been studied in greater detail in Crohn's disease.
Celulele implicate in raspunsul imun sunt activate si expresia citokinelor proinflamatorii si a chemokinelor este upregulated in BII. Different responses to transient intestinal injury in genetically susceptible versus genetically resistant hosts.
After nonspecific injury from an environmental trigger, such as an infection or exposure to a nonsteroidal antiinflammatory drug NSAIDnormal hosts rapidly repair the mucosal defect and downregulate innate and T-cell immune responses with no residual tissue damage. By contrast, individuals in whom immunoregulation, epithelial barrier function or bacterial killing is defective, develop chronic inflammation that is mediated by aggressive T-cell responses to dysbiosis crohns disease hpv hair removal antigens.