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PubMed2002

Faecal calprotectin: a marker of inflammation throughout the intestinal tract.

Only a small proportion of patients with abdominal discomfort have organic disease, but a correct diagnosis can seldom be made by simple clinical examination. Additional diagnostic procedures must be employed, but these are expensive and demanding and carry a certain risk. Assessment of faecal concentrations of the neutrophil granulocyte-derived protein calprotectin can be used as a screening test--an 'ESR of the gut'--to select patients for further examination. The test can be performed on 1-2 g of random stool samples that can be sent to the laboratory by ordinary mail since the protein is remarkably stable in stools. The test has high sensitivities and specificities for gastrointestinal cancers and inflammatory bowel disease (IBD). Faecal calprotectin levels reflect the disease activity in IBD and can be used to monitor the response to treatment and detect relapses.

Biomarkers↗
PubMed2003

Eosinophilic myenteric ganglionitis is associated with functional intestinal obstruction.

The diagnostic features and clinical course of three children (aged 1 month to 15 years) with severe functional intestinal obstruction and inflammation of the colonic lamina propria and myenteric plexus are described. The myenteric inflammatory infiltrate was eosinophil predominant with none of the immunological characteristics of lymphocytic ganglionitis. Neurones in the myenteric ganglia expressed the potent eosinophil chemoattractant interleukin 5. None responded to dietary exclusion but all three responded symptomatically to immunosuppression/anti-inflammatory treatments. Eosinophilic ganglionitis is associated with a pseudo-obstructive syndrome which is amenable to anti-inflammatory treatment.

Adolescent↗
PubMed1994

Radiation risks from imaging of intestinal and abdominal inflammation.

Most abdominal imaging procedures involve some radiation dose to the patient. The types of radiation-induced harm from these techniques are described. The dose received from each of these techniques in clinical practice is thought to be below the threshold required to cause developmental abnormalities in pregnancy. According to the present state of knowledge, there is no significant risk of genetic damage to the patient from any of these procedures. Organs vary considerably in their sensitivity to radiation-induced cancer. The effect of radiation on any organ depends on the radiation dose to that particular organ only. The most radiosensitive organs are bone marrow, lung, stomach and large bowel. The macroscopic and microscopic distribution of radiation dose is discussed for all of the various imaging techniques. There is a large dose variation between individual patients and the mean dose received from each procedure is similar for each of the imaging techniques described, the mean radiation dose is low and the decision as to which test to choose depends more on the diagnostic value of each particular procedure.

Abdomen↗
PubMed1998

Enantiomers of flurbiprofen can distinguish key pathophysiological steps of NSAID enteropathy in the rat.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal damage by a non-prostaglandin (PG) dependent "topical" action and by inhibiting cyclooxygenase. AIMS: To discriminate between these two effects by studying some key pathophysiological steps in NSAID enteropathy following administration of (R)- and (S)-flurbiprofen, the racemic mixture, and an uncoupler, dinitrophenol. METHODS: The effects of dinitrophenol, racemic, (R)-, and (S)-flurbiprofen on mitochondria were assessed in vitro and on key pathophysiological features of small intestinal damage in vivo (ultrastructure by electron microscopy, mucosal prostanoid concentrations, intestinal permeability, inflammation, and ulcer count) in rats. RESULTS: All the drugs uncoupled mitochondrial oxidative phosphorylation in vitro, caused mitochondrial damage in vivo, and increased intestinal permeability. Dinitrophenol and (R)-flurbiprofen caused no significant decreases in mucosal prostanoid concentrations (apart from a decrease in thromboxane (TX) B2 concentrations following (R)-flurbiprofen) while racemic and (S)- flurbiprofen reduced mucosal prostanoids significantly (PGE, TXB2, and 6-keto-PGF1alpha concentrations by 73-95%). Intestinal inflammation was significantly greater following administration of (S)-flurbiprofen and racemate than with dinitrophenol and (R)-flurbiprofen. No small intestinal ulcers were found following dinitrophenol or (R)-flurbiprofen while both racemic and (S)-flurbiprofen caused numerous ulcers. CONCLUSIONS: Dinitrophenol and (R)-flurbiprofen show similarities in their actions to uncouple mitochondrial oxidative phosphorylation in vitro, alter mitochondrial morphology in vivo, increase intestinal permeability, and cause mild inflammation without ulcers. Concurrent severe decreases in mucosal prostanoids seem to be the driving force for the development of severe inflammation and ulcers.

Animals↗
PubMed2006

Attenuation of colonic inflammation by PPARgamma in intestinal epithelial cells: effect on Toll-like receptor pathway.

The peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor highly expressed in the colon and playing an anti-inflammatory role through inhibition of the NF-kappaB pathway. Toll-like receptor 4 (TLR4) has been known to mediate LPS-induced cellular signaling through activation of NF-kappaB pathway in intestinal epithelial cells. The aims of this study were to evaluate attenuation of inflammation by PPARgamma in intestinal epithelial cells and to study the possible relation between PPARgamma and TLR4. HT-29 human epithelial cells were stimulated with LPS (20 microg/ml) and PPARgamma ligand, 15d-PGJ2 (10 microM), or with LPS (20 microg/ml) alone for 24 hr. COX-2, IL-8, TLR4, and PPARgamma mRNA expression was assessed by RT-PCR. IL-8 protein levels and TLR4 protein expression were analyzed by ELISA and Western blot, respectively. To evaluate the action mechanisms of PPARgamma ligand, Western blot analysis for IkappaBalpha degradation was performed. Costimulation with LPS and PPARgamma ligand in comparison to LPS stimulation alone (1) decreased COX-2, IL-8 mRNA expression and IL-8 protein secretion, (2) decreased TLR4 mRNA and protein expression, and (3) decreased PPARgamma mRNA expression. PPARgamma ligand delayed LPS-induced IkappaBalpha degradation. These findings suggest that PPAR-gamma ligands suppress inflammation in intestinal epithelial cells. PPARgamma and TLR, these two antagonistic signaling pathways in intestinal epithelial cells may be partially cross-linked.

Blotting, Western↗
PubMed1990

Hepatic inflammation in rats with experimental small intestinal bacterial overgrowth.

Hepatobiliary inflammation and other extraintestinal manifestations accompany certain intestinal disorders, perhaps because of proliferation or enhanced transport of luminal bacteria or their phlogistic cell-wall components. Using jejunal self-filling blind loops to create small bowel bacterial overgrowth, we compared biochemical and histological evidence of hepatic inflammation in 3 rat strains chosen for their variable inflammatory responses to bacterial cell wall polymers. Lewis and Wistar rats developed weight loss, hepatomegaly, and hepatic inflammation 4 and 12 wk, respectively, after creation of SFBL. Plasma aspartate aminotransferase levels in Lewis rats 4 wk (578 +/- 77 U/L) and Wistar rats 12 wk (220 +/- 35 U/L) after self-filling blind loops were significantly greater than in rats with self-emptying blind loops (112 +/- 24 U/L, p less than 0.001; 104 +/- 22, p less than 0.05) or sham-operated Lewis (84 +/- 24, p less than 0.001) or Wistar (78 +/- 10, p less than 0.001) rats. Randomized comparison using a histology grading score showed abnormalities that paralleled aminotransferase values. Lewis and Wistar rats with self-filling blind loops had hepatic injury with bile duct proliferation, fibrosis and acute and chronic periportal and focal parenchymal inflammation. Lewis and Wistar rats with self-emptying blind loops developed occasional mild histologic lesions. 50% of Lewis rats with self-filling blind loops for 4 wk died compared with only 15% in other groups. However, Buffalo rats with self-filling blind loops developed no weight loss, hepatomegaly, or hepatic injury. Anaerobic cultures of blood, peritoneum and liver were negative in all strains. Diet-restricted, sham-operated Wistar rats with weights similar to the Wistar rats with self-filling blind loops did not develop histologic abnormalities or elevated aminotransferase levels (76 +/- 31 U/L). These results show that experimental small bowel bacterial overgrowth causes significant hepatic inflammation leading to fibrosis in susceptible rat strains. Caloric deprivation and hepatic bacterial invasion are not etiologically responsible. We suggest that bacterial cell wall polymers or other bacterial toxins from the blind loop cause hepatic lesions in genetically susceptible hosts.

Animals↗
PubMed2006

Effects of sphingosine-1-phosphate and ceramide-1-phosphate on rat intestinal smooth muscle cells: implications for postoperative ileus.

Postoperative ileus, a major cause of morbidity after abdominal surgery, is characterized by intestinal dysmotility and inflammation. The aim was to investigate the involvement of sphingolipids in postoperative intestinal inflammation using a standardized rat model of intestinal surgical manipulation. Sphingolipid analysis (ESI-MS) of intestinal muscularis after manipulation revealed a time-dependent increase of sphingosine 1-phosphate (S1P) and of ceramide 1-phosphate (C1P). We therefore established a culture system of primary rat intestinal smooth muscle cells and examined the potential role of these sphingolipids in intestinal inflammation. Incubation of cells with either of the two sphingolipid-phosphates resulted in an elevated production of PGE(2). Further analysis revealed that S1P enhances cyclooxygenase 2 (COX-2) expression whereas C1P increases release of arachidonic acid, indicating an enhanced phospholipase A(2) activity. S1P-induced COX-2 expression was pertussis toxin sensitive, suggesting the involvement of Gi/o protein-coupled S1P receptors. Further downstream mediators of S1P induced COX-2 expression appear to be extracellular regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). Collectively, our results demonstrate that intestinal smooth muscle cells represent a major target for both C1P and S1P activity. Thus, the sustained elevated concentration of the two bioactive sphingolipids in this tissue could at least in part explain postoperative intestinal dysmotility.

Animals↗
PubMed1999

Myeloperoxidase activity of the large intestine in an equine model of acute colitis.

OBJECTIVE: To determine whether quantification of myeloperoxidase (MPO) activity could be a useful laboratory technique to detect granulocyte infiltration in equine intestinal tissues. SAMPLE POPULATION: Intestinal tissue (inflamed or healthy) collected from 16 age- and sex-matched Shetland Ponies. PROCEDURE: Intestinal tissue MPO activity was determined, and histologic assessment of adjacent specimens from healthy and inflamed intestine was done. RESULTS: Intestinal tissue MPO activity and histopathologic score increased with time after castor oil challenge and peaked at 16 hours in an equine diarrhea model in which individual ponies provided their own control tissues. CONCLUSIONS: Intestinal tissue inflammation scores correlated positively with tissue MPO activity in adjacent specimens. CLINICAL RELEVANCE: Tissue MPO assay may be a useful laboratory tool to quantify intestinal mucosal inflammation in ponies.

Animals↗
PubMed2003

Dextran sulfate sodium-induced inflammation is enhanced by intestinal epithelial cell chemokine expression in mice.

Dextran sulfate sodium (DSS) induces an inflammatory bowel disease-like colitis in animals. To determine the contribution of epithelium to inflammation in the intestine, we examined the effects of DSS in transgenic mice that specifically secrete macrophage inflammatory protein-2 (MIP-2) from the intestinal epithelium. We first confirmed the production of MIP-2 from intestinal epithelial cells by Western blots in transgenic mice. MIP-2 transgenic mice were therefore an appropriate model to examine the role of epithelial cell chemokines in an inflammatory state induced by DSS. We then examined the neutrophil migration into the intestine and the effect of DSS on this migration by myeloperoxidase staining. There was an increase of myeloperoxidase-positive neutrophils in the intestine from wild-type and transgenic mice after the DSS treatment. Furthermore, the increase of neutrophils under stimulation with DSS was confirmed quantitatively by measuring specific tissue myeloperoxidase activities. It was significantly greater in DSS-treated MIP-2 transgenic mice than in wild-type mice in both the small intestine and colon. These results suggest that the inflammatory effects of DSS on both small intestine and colon are enhanced by MIP-2 secreted by epithelial cells in the transgenic mice. In conclusion, intestinal epithelial cells can act in concert with other inflammatory stimuli in maintaining inflammation.

Animals↗
PubMed2026

Eagle-Derived Weissella confusa EG05 Prevents LPS-Induced Enteritis Through Modulation of Inflammation, Gut Barrier, And Microbiota.

Intestinal enteric inflammation can seriously harm animal health and lead to massive economic losses in livestock production. Probiotics have become a promising alternative to antibiotics for preventing and controlling enteritis. In this study, a novel lactic acid bacterium (LAB) was isolated from eagle feces and identified as Weissella confusa EG05 (W. confusa EG05), and its probiotic characteristics and protective effects on lipopolysaccharide (LPS)-induced enteritis in mice were evaluated. In vitro experiments showed that W. confusa EG05 has strong antimicrobial activity against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus), good tolerance to acidic and bile salt conditions, high auto-aggregation ability and surface hydrophobicity, and no hemolytic activity. Whole-genome analysis further confirmed its safety and probiotic potential by revealing genes involved in adhesion, immune regulation, and stress tolerance. In mouse experiments, pretreatment with W. confusa EG05 alleviated LPS-induced intestinal pathological damage, inhibited the secretion of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-6), promoted the expression of anti-inflammatory cytokine IL-10, enhanced the activities of antioxidant enzymes, and up-regulated the expression of tight junction proteins (Occludin, ZO-1). In addition, W. confusa EG05 restored gut microbiota homeostasis disturbed by LPS, increasing the abundance of beneficial genera and decreasing harmful bacteria. Taken together, these results suggest that W. confusa EG05 can effectively prevent LPS-induced enteritis in mice by modulating the inflammatory response, enhancing antioxidant capacity, protecting the intestinal barrier and the reshaping gut microbiota. These results indicate that W. confusa EG05 exhibits prominent probiotic potential in mouse models, providing a strain resource for the future development of microecological preparations.

Weissella confusa EG05↗
PubMedDate not supplied

The interleukin-2-deficient mouse model.

Interleukin-2-deficient (IL-2(-/-)) mice develop colitis with striking clinical and morphological similarities to ulcerative colitis. Since transport and barrier properties are impaired in ulcerative colitis, we studied transport and barrier functions in IL-2(-/-) mice in order to gain insight for the first time into the general pathomechanisms of disturbed transport and barrier function of the intestine during inflammation. Alternating current impedance analysis was used to determine tissue conductance in the inflamed proximal colon of IL-2(-/-) mice and to discriminate between pure epithelial and subepithelial conductance. Surprisingly, epithelial conductance was not increased but diminished in IL-2(-/-) mice compared to controls (20.2 +/- 1.3 versus 28.8 +/- 2.8 mS/cm(2)). Concomitantly, conductance of the subepithelial tissue layers was decreased in IL-2(-/-) mice as a result of edema and infiltration with inflammatory cells. In the distal colon, electrogenic Na(+) transport (J(Na)) mediated by the epithelial Na(+) channel (ENaC) was measured 8 h after stimulation with 3.10(-9) M aldosterone in vitro as the drop in I(SC) (short circuit current) after addition of 10(-4) M amiloride. In controls, J(Na) was 6.9 +/- 0.9 micromol x h(-1) x cm(-2), whereas it was abolished in IL-2(-/-) mice. In conclusion, the inflamed colon of IL-2(-/-) mice exhibits a severe disturbance in Na(+) uptake via the ENaC in the absence of a barrier defect. Thus, reduced expression of active absorptive transport and not a barrier defect is responsible for the diarrhea in this model of intestinal inflammation. This makes this model suitable for studying the general pathomechanisms of the inflammatory downregulation of intestinal transport proteins.

Aldosterone↗