The most commonly accepted hypothesis on the IBD etiology is that abnormalities in the innate immune response by the mucosa cause a loss of tolerance to commensal microbiota and alterations in the composition of the gut microbiota.
H. pylori infection of the gastric mucosa causes a chronic local inflammatory cell infiltration, which in turn gives rise to a serological response, in which H. pylori specific antibodies are almost always detectable [ 8, 9].
It is possible that 3-MF after bioactivation is covalently binding to proteins of the mucosa, causing both chemical injury and a protein-hapten reaction resulting in airway inflammation and a hypersensitivity pneumonitis.
Cytotoxic chemotherapy agents have a direct effect on the GI mucosa causing inflammation, 11 13 oedema, ulceration and atrophy.
Damage to intestinal mucosa in celiac disease (CD) is mediated both by inflammation due to adaptive and innate immune responses, with IL-15 as a major mediator of the innate immune response, and by proliferation of crypt enterocytes as an early alteration of CD mucosa causing crypts hyperplasia.
Damage to the intestinal mucosa in CD is mediated both by inflammation due to the adaptive and innate immune responses (with IL-15 as a major mediator of the innate immune response) and by proliferation of crypt enterocytes as an early alteration of CD mucosa causing crypt hyperplasia [4] [6].
Normal result of D-xylose test was helpful as it suggested normalization of intestinal mucosa; D-xylose test has a high sensitivity to detect abnormal mucosa causing MAS [ 11].
The implants generally involve the serosal surface but may invade the underlying muscular and submucosal layers; only rarely implants erode the mucosa causing cyclic rectal bleeding.
The reperfused intestine may have a different pattern [21], depending on degree of microvascular wall damage, blood plasma, contrast medium, or red blood cells may extravasate through the disrupted vascular wall and mucosa, causing considerable bowel wall thickening and bloody fluid filling of the bowel lumen [16, 21].
Substances released from these materials into saliva can then diffuse across the oral or gastrointestinal mucosa, causing adverse reactions [ 9– 11].
