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Results for “Intestinal Inflammation”

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At least 1,711 records · Page 95Linked to original sources
PubMed2000

The I kappa B/NF-kappa B system: a key determinant of mucosalinflammation and protection.

The ubiquitous transcription factor NF-kappa B is a central regulator of the transcriptional activation of a number of genes involved in cell adhesion, immune and proinflammatory responses, apoptosis, differentiation, and growth. Induction of these genes in intestinal epithelial cells (IECs) by activated NF-kappa B profoundly influences mucosal inflammation and repair. NF-kappa B activation requires the removal of I kappa B from NF-kappa B by inducible proteolysis, which liberates this transcription factor for migration to the nucleus, where it binds to kappa B-regulatory elements and induces transcription. I kappa B alpha degradation is incomplete and delayed in IECs, resulting in buffered responses to luminal stimuli. The stimulatory environment partially determines whether the effect of NF-kappa B is protective or deleterious for the host. kappa B-dependent proinflammatory gene expression, particularly chemokines, major histocompatibility complex class II antigens, and adhesion molecules may be extremely important in early protective responses to mucosal pathogens but, when dysregulated, could lead to the development of chronic inflammation, as seen in inflammatory bowel diseases. The key role of NF-kappa B in regulating expression of a number of proinflammatory genes makes this protein an attractive target for selective therapeutic intervention.

Animals↗
PubMed2005

Events at the host-microbial interface of the gastrointestinal tract. II. Role of the intestinal epithelium in pathogen-induced inflammation.

An immense number of bacteria reside within the intestinal lumen. The task of appropriately identifying and responding to microbial threats lies primarily with the single layer of cells that line the intestinal tract. Intestinal epithelial cells have developed a number of strategies aimed at identifying microorganisms and eliciting the appropriate inflammatory response. The pathogen recognition mechanisms and the signaling and inflammatory events that ensue within the intestine are the focus of this review.

Animals↗
PubMed2001

Epidemiology and differential diagnosis of NSAID-induced injury to the mucosa of the small intestine.

Non-steroidal anti-inflammatory drugs cause small-bowel inflammation in about 60% of patients receiving these drugs long-term. The inflammation is associated with small intestinal bleeding, protein loss, ulcers and occasionally strictures. Treatment options for NSAID enteropathy include metronidazole, sulphasalazine and misoprostol, and some patients may require surgery. The diagnosis of NSAID enteropathy is not always straightforward. It is especially difficult to differentiate it from the ileitis associated with spondylarthropathy and, at times, that of Crohn's disease. An investigational algorithm is suggested for this purpose. In the last decade a number of small-bowel diseases have been identified, where none were thought to exist, because of the increasing use of enteroscopy and new sensitive tests for intestinal inflammation. Optimal treatments of these conditions are still to be studied.

Algorithms↗
PubMed2004

Elevated vasoactive intestinal peptide concentrations in patients with irritable bowel syndrome.

The aim was to assess the roles of gut hormones and immune dysfunction in irritable bowel. In Study I, rectal mucosal samples examined blindly showed no histological evidence of inflammation in 16 irritable bowel patients compared to 17 healthy controls. The proinflammatory mediators interleukin-1beta and prostaglandin E2 also failed to show evidence of inflammation. Vasoactive intestinal peptide was elevated in irritable bowel (P = 0.01), but substance P, calcitonin gene-related peptide, and somatostatin levels were similar to control values. In Study II, 30 irritable bowel patients had elevated (P = 0.002) plasma concentrations of vasoactive intestinal peptide compared to 30 controls, and peptide levels were unrelated to whether the patient's predominant bowel habit was constipation, diarrhea, or both in alternation. In conclusion, no evidence of inflammation was detected in irritable bowel patients, but elevated vasoactive intestinal peptide concentrations were observed in both studies and might represent a potential diagnostic tool for irritable bowel syndrome.

Adult↗
PubMed1982

Klebsiella pneumoniae enterotoxin. III. Effect of Klebsiella pneumoniae enterotoxin on the intestinal transport and histopathological changes in rabbit ileal loop.

Klebsiella pneumoniae strain B-5-1 was used to study the effect of its enterotoxin on the intestinal transport and histopathological changes in the rabbit ileal loop. Enterotoxin increased the net flux of water and of electrolytes. Increased amounts of phospholipids and proteins were also detected together with structural and functional abnormalities in the ileum. All these suggest that K. pneumoniae enterotoxin not only induce a net flux of fluid and imbalance of electrolytes but also damages the intestinal structure.

Animals↗
PubMed1984

The experimental basis of intestinal suturing. Effect of surgical technique, inflammation, and infection on enteric wound healing.

Factors that incite inflammation at the healing wound prolong the lag period of wound healing and delay the return of strength at the suture line. Inflammation activates bowel-wall collagenase, which degrades the collagen within the wound, eroding the foundation in which sutures are anchored. Experimental studies have compared the impact of various surgical techniques. Sutures placed by hand uniformly invoke an inflammatory response because dragging the thread through the bowel wall injures tissue. Single-layer anastomoses heal more rapidly than double-layer suture lines. The inner layer causes avascular necrosis of the inverted cuff. Experimental studies have not clearly shown the superiority of inverting suture lines over everting ones. Experimental studies done over the last century indicate that the single-layer inverting anastomosis recommended by Lembert and Halstead adequately compensates for enteric wound weakness during the lag period. Other techniques of sewing an anastomosis provide no clear advantage. Other factors that incite inflammation also delay enteric wound healing. Debris, necrotic tissue, or infection illicit an inflammatory response with detrimental effects on the anastomosis. Antibiotics, by assisting in the control of infection or by minimizing the size of an inoculum, help speed healing. Stapling devices violate many of the doctrines of intestinal suturing. Experimental studies suggest, however, that staple lines incite a minimal inflammatory response. Consequently, wounds closed with stapling devices regain strength more rapidly than those closed with traditional surgical techniques.

Animals↗
PubMed2004

Signaling for inflammation and repair in inflammatory bowel disease.

In patients with inflammatory bowel diseases (IBD) the immune system leads to the polarization of intestinal immune cells towards a T helper one (Th1) pro-inflammatory response. The immunologic factors intervene in intestinal homeostasis and initiate the development of intestinal mucosal inflammation. Cytokines, which are important regulators of inflammation and repair as wells as leukocyte trafficking have become apparent as key immune molecules in the pathogenesis of IBD. In this review, recent advances in our understanding of the cytokine involvement in inflammation and repair in patients with ulcerative colitis (UC) and Crohn's disease (CD) are discussed. Knowledge of objective evidence of inflammatory activity may allow targeted treatment at an earlier stage to avoid the relapse, as well as assessment of new therapeutic strategies for maintenance of remission.

Apoptosis↗