Relation of peroxidase activity in gut mucosa to inflammation

Smith, Joseph Wayne; Castro, Gustavo

doi:10.1152/ajpregu.1978.234.1.r72

Cited by 73 publications

(50 citation statements)

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“…The maximum score is 13, to which is added the thickness of the colonic wall measured in millimeters. A section of the colon 2 cm proximal to the anus was removed and stored at Ϫ20°C for later assessment of myeloperoxidase activity (34,35). Wet and dry weights were obtained on the remaining left colon to determine intestinal tissue edema.…”

Section: Methodsmentioning

confidence: 99%

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Sawczenko

Azooz

Paraszczuk

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

111

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Inflammatory diseases frequently impair linear growth. Crohn's disease inhibits growth in up to one third of affected children. In rats with trinitrobenzenesulphonic acid-induced colitis, 40% of growth impairment is attributable to inflammation, with the rest being due to undernutrition. In transgenic mice without inflammation, raised IL-6 retards growth, suppressing insulin-like growth factor (IGF)-I. We hypothesized that IL-6, induced by intestinal inflammation, suppresses growth and inhibits IGF-I expression. Therefore, an anti-IL-6 Ab was given to rats with trinitrobenzenesulphonic acid colitis. The Ab did not improve nutrient intake or decrease inflammation compared with untreated disease controls, but it significantly restored linear growth (P ‫؍‬ 0.023) and increased IGF-I (P ‫؍‬ 0.05). In humans, the IL-6 ؊174 G͞C promoter polymorphism affects IL-6 transcription, with the GG genotype inducing the greatest IL-6 levels. Because IL-6 is increased in Crohn's disease, we further hypothesized that growth failure would vary with the IL-6 ؊174 genotype. At diagnosis, among 153 children with Crohn's disease, those with the IL-6 GG genotype were more growthretarded than those with the GC or CC genotypes (height SD score, ؊0.51 vs. ؊0.10; P ‫؍‬ 0.031). Also, the patients with the IL-6 GG genotype had higher circulating levels of C-reactive protein, an IL-6-induced product (36 vs. 18 mg͞dl, P ‫؍‬ 0.028). However, their risk of developing Crohn's disease was similar to other genotypes when compared with 351 healthy controls (P ‫؍‬ 0.7). Thus, the IL-6 ؊174 genotype mediates growth failure in children with Crohn's disease.Crohn's disease ͉ height ͉ insulin-like growth factor I ͉ C-reactive protein ͉ food intake

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Section: Methodsmentioning

confidence: 99%

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Sawczenko

Azooz

Paraszczuk

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

111

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“…Three days after intrarectal administration of DNBS, the colon was removed, snap frozen in liquid nitrogen, and stored at Ϫ70°C. Samples were weighed, and MPO was measured using a technique described before (47). MPO activity is reported as units of MPO per milligram of wet tissue.…”

Section: Methodsmentioning

confidence: 99%

Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

et al. 2002

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Epidemiological studies suggest that inflammatory bowel disease (IBD) is common in developed countriesIn the present study, we investigated the effect of polarizing the immune response toward the Th2 type, using intestinal nematode infection, on subsequent experimental colitis. Mice were infected with the intestinal nematode Trichinella spiralis and allowed to recover before colitis was induced with dinitrobenzene sulfonic acid. The mice were sacrificed postcolitis to assess colonic damage macroscopically, histologically, and by myeloperoxidase (MPO) activity and Th cytokines. Prior nematode infection reduced the severity of colitis both macroscopically and histologically together with a decreased mortality and was correlated with a downregulation of MPO activity, Th1-type cytokine expression in colonic tissue, and emergence of a Th2-type immune response. These results indicate a protective role of nematode infection in Th1 cell-driven inflammation and prompt consideration of a novel therapeutic strategy in IBD based on immunological distraction.

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“…MPO is an enzyme found within the azurophilic granules of neutrophils and other cells of myeloid origin. It has been demonstrated previously that these levels reflect the state of inflammation in the mucosa of the intestine [21,22]. Tissue samples were weighed and stored at −20°C until assayed within a week using a well-established assay [23].…”

Section: Measurement Of Neutrophil Infiltrationmentioning

confidence: 99%

An angiotensin II receptor antagonist reduces inflammatory parameters in two models of colitis

Santiago

Rivera

Ferder

et al. 2008

Regulatory Peptides

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Little is known about the effects of the proinflammatory hormone Angiotensin II (Ang II) in inflammatory bowel disease. The aim of this study was to evaluate the effect of Valsartan (Diovan), an Ang II receptor antagonist, in two models of colitis.METHODS-Colitis was induced in Sprague-Dawley rats by administration of trinitrobenzene sulfonic acid (TNBS; 30mg in 50% ETOH ic) or 5% Dextran Sulphate Sodium (DSS) in drinking water ad libitum for 5 days. Valsartan was administered orally in drinking water (160mg/L) during thirty days prior to the induction of the colitis, and for 5 days after. All animals were evaluated for weight change, diarrhea, myeloperoxidase activity, macroscopic and microscopic damage. Cytokine levels in the colon were measured by ELISA, real time RT-PCR and immunohistochemistry.RESULTS-In the TNBS model, Valsartan reduced the macroscopic damage score, significantly decreased the microscopic damage (p<0.01), and accelerated weight gain after colitis. In the DSS colitis model, Valsartan treated animals had less diarrhea and microscopic damage. Valsartan reduced the protein levels of TGFβ (p<0.05), and IL-18 in the TNBS model, and led to over-expression of IL-10 mRNA in the DSS model.CONCLUSION-These data demonstrate a possible anti-inflammatory effect for Valsartan in colitis.

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Relation of peroxidase activity in gut mucosa to inflammation

Cited by 73 publications

References 0 publications

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the –174 IL-6 G/C polymorphism in children

Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

An angiotensin II receptor antagonist reduces inflammatory parameters in two models of colitis

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