fibrin and Colitis

Topics: Adult; Aged; Autopsy; Brain; Central Venous Pressure; Colitis; Colon; Enteritis; Female; Fibrin; Heart Ventricles; Hemorrhage; Humans; Kidney; Kidney Glomerulus; Kidney Tubules; Liver; Lung; Male; Middle Aged; Myocardium; Necrosis; Pancreas; Shock; Thrombosis

Mucosal repair after acute colonic inflammation is central to maintaining mucosal homeostasis. Failure of mucosal repair often leads to chronic inflammation, sometimes associated with inflammatory bowel disease (IBD). The adenomatous polyposis coli (APC) tumor suppressor gene regulates the Wnt signaling pathway, which is essential for epithelial development, and inactivation of APC facilitates colorectal cancer. Our previous study suggested that APC is involved in pathogenesis of colonic inflammation; however, its role in mucosal repair remains unknown. In this article, we report that colitis induced by dextran sodium sulfate persisted with delayed mucosal repair in Kyoto Apc Delta (KAD) rats lacking the APC C terminus. Defects in the repair process were accompanied by an absence of a fibrin layer covering damaged mucosa and reduced microvessel angiogenesis. APC was up-regulated in vascular endothelial cells (VECs) in inflamed mucosa in KAD and F344 (control) rats. The VECs of KAD rats revealed elevated cell adhesion and low-branched and short-length tube formation. We also found that DLG5, which is associated with IBD pathogenesis, was up-regulated in VECs in inflamed mucosa and interacted with the C terminus of APC. This finding suggests that loss of interaction between the APC C terminus and DLG5 affects VEC morphology and function and leads to persistence of colitis. Therefore, APC is essential for maintenance of intestinal mucosal homeostasis and can consequently contribute to IBD pathogenesis.

Topics: Adenomatous Polyposis Coli Protein; Animals; Cell Adhesion; Colitis; Colon; Cytokines; Dextran Sulfate; Endothelial Cells; Epithelium; Fibrin; Inflammation; Inflammation Mediators; Intestinal Mucosa; Male; Membrane Proteins; Microtubule-Associated Proteins; Neovascularization, Physiologic; Protein Binding; Protein Transport; Rats; Rats, Inbred F344; Time Factors; Wnt Signaling Pathway; Wound Healing

E. coli O157:H7 may cause hemorrhagic colitis resembling ischemic colitis. Diagnosis is usually made by finding sorbitol-negative colonies on MacConkey agar that react with O157 and H7 antisera. Most ischemic colitis is idiopathic, but some may be caused by E. coli O157:H7, inasmuch as this organism can produce fibrin thrombi in colon vasculature. The objectives of this study were to determine whether E. coli O157:H7 infection can be diagnosed retrospectively from paraffin blocks of colon sections and whether an association exists between E. coli O157:H7 infection and colonic ischemia.. Paraffin-embedded sections of normal colon (n = 2) and various colitides [ischemic (n = 11), E. coli O157:H7 (n = 2), IBD (n = 8) and pseudomembranous (n = 3)] were used. Sections were deparaffinized, rehydrated, incubated with 3% peroxide in methanol, rinsed, and incubated with peroxidase-labeled antibody isolated from goats immunized with whole E. coli O157:H7. Sections were stained with peroxidase chromagen reagent and counterstained with hematoxylin. Coarse, granular, orange-brown staining was considered positive. To determine the localization of the chromagen deposits, three cases that stained positive, including one of the culture-proved E. coli O157:H7 colitis and two of colonic ischemia, were processed for electron microscopy.. Both cases (100%) of E. coli O157:H7 colitis and three of 11 (27.3%) cases of ischemic colitis stained positive by light microscopy. In one culture-proved case, electron microscopy demonstrated staining of bacillary structures; in two cases of colonic ischemia, extensive deposits of chromagen material were present that were associated neither with inflammatory cells nor with bacterial forms.. Immunoperoxidase staining of archival sections may be used to diagnose E. coli O157:H7 infection. An etiological role for this organism is possible in some cases of colonic ischemia.

Topics: Aged; Antibodies, Bacterial; Chromogenic Compounds; Colitis; Colitis, Ischemic; Colon; Coloring Agents; Enterocolitis, Pseudomembranous; Escherichia coli Infections; Escherichia coli O157; Female; Fibrin; Gastrointestinal Hemorrhage; Hematoxylin; Humans; Immunoenzyme Techniques; Inflammatory Bowel Diseases; Male; Microscopy, Electron; Middle Aged; Paraffin Embedding; Retrospective Studies; Thrombosis

A 48-year-old man with accelerated hypertension developed right-sided ischemic colitis. There was no evidence of another cause of vascular inadequacy. Microscopically, the bowel showed ischemic alterations of different stages. The arterial alterations of different stages. The arterial vessels showed minimal changes. In older lesions, fibrosis was prominent and the mucosa was atrophic. In more recent lesions, some vessels of the submucosa were plugged with fibrin and the overlying mucosa was infiltrated by nonorganized hemorrhage and cellular elements.

Topics: Arteries; Atrophy; Colitis; Colon; Fibrin; Gastrointestinal Hemorrhage; Humans; Hypertension; Intestinal Mucosa; Ischemia; Male; Middle Aged

Rectal biopsies from five patients with clindamycin-associated colitis were studied with the intention of identifying fibrin thrombi in capillaries. Capillary thrombosis was present in all five cases, three with pseudomembranous colitis and two with non-specific colitis. The significance of capillary thrombosis and its relationship to other ischaemic lesions of the gut are discussed.

Topics: Aged; Biopsy; Clindamycin; Colitis; Diarrhea; Female; Fibrin; Humans; Intestinal Mucosa; Male; Middle Aged; Rectum; Thrombosis

Topics: Animals; Blood Vessels; Cell Membrane; Colitis; Colitis, Ulcerative; Colon; Crohn Disease; Cytoplasm; Disease Models, Animal; Edema; Endotoxins; Epithelium; Escherichia coli Infections; Fibrin; Intestinal Mucosa; Lymphatic System; Macrophages; Microscopy, Electron; Organoids; Phagocytosis; Swine

Topics: Adenosine Triphosphatases; Blood Platelets; Colitis; Colitis, Ulcerative; Dihydrolipoamide Dehydrogenase; Endocarditis; Fibrin; Geriatrics; Glomerulonephritis; Histocytochemistry; Humans; Mitral Valve; Pathology; Polysaccharides; Rheumatic Heart Disease; Thrombosis