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Celiac disease is a slowly progressing intestinal reaction to gluten.
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Sc (strain CNCM I-3856) displays multiple immuno-modulatory effects at the molecular level in IPEC-1 cells suggesting that Sc may influence intestinal inflammatory reaction.
These two animal models of sensitization can produce an IgE-dependent intestinal allergic reaction yielding an anaphylaxis-dependent increase in intestinal permeability [ 5, 14].
Oxytetracycline has a specific ability to chelate with divalent metal ions [ 3, 1], and an intestinal chelation reaction which inactivated the oxytetracycline excreted to the gut probably occurred.
Although anaphylactic reactions induced by intraperitoneal [ 27] or intravenous [ 28] administration of antigen are generally accompanied by marked and rapid hemoconcentration, the intestinal hypersensitivity reaction did not produce significant modification of hematocrit, even with the observed increases in vascular permeability.
Codfish allergens have a grossly reduced ability to trigger an intestinal allergic reaction when they are digested [ 11], and incomplete gastric digestion of cod allergens represents a risk factor for allergen-induced anaphylaxis [ 12].
A previously published mouse reconstruction was expanded by intestinal transport reactions based on literature and was improved by correcting for duplicate or nonfunctional reactions and erroneous GPRs.
Additionally, circulating immune cells are able to infiltrate the gut tissues participating in intestinal immune reactions, as occurs with vertebrate lymphocytes and very likely with invertebrate coelomocytes.
Severe late intestinal radiation reactions were recorded in about 10% [ 28].
PBMCs from a group (n = 27) of RC patients with an adverse (grade 2 3) clinical gastro-intestinal (GI) reaction to RT have also been retrospectively analyzed.
In literature reviews, severe late intestinal radiation reactions were recorded in about 10%, and were associated with pelvic boost and previous second-look laparotomy.
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