Abstract
Tumour necrosis factor-α expression may be increased in segmental colitis associated with diverticulosis.
To assess tumour necrosis factor-α expression in segmental colitis associated with diverticulosis in relation with the severity of the endoscopic damage....
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PMID: 21195685
PDF is available here.
Abstract
Serine proteases are important in the pathogenesis of intestinal inflammation. Recent studies have shown that nafamostat mesilate (NM) can inhibit the colonic mucosal inflammation induced by TNBS in rats. The aim of this study was to investigate the anti-inflammatory effects of NM on...
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PMID: 21187179
PDF is available here.
Abstract
Silymarin has intracellular antioxidant property and inhibits activation of nuclear factor-κB (NF-κB) in low concentrations and reduces tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 levels, cyclooxygenase (COX), and angiogenesis. Selenium is one of the necessary...
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PMID: 21247366
PDF is available here.
F Meylan,
Y-J Song,
I Fuss,
S Villarreal,
E Kahle,
I-J Malm,
K Acharya,
H L Ramos,
L Lo,
M M Mentink-Kane,
T A Wynn,
T-S Migone,
W Strober and
R M Siegel
Abstract
We generated transgenic mice that constitutively express TL1A in T cells or dendritic cells. These mice spontaneously develop IL-13-dependent inflammatory small bowel pathology that strikingly resembles the intestinal response to nematode infections. These changes were dependent on the presence of a...
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PMID: 20980995
PDF is available here.
Abstract
We have found that many of these approaches are encumbered with their own limitations. Therefore, we sought to develop a relatively simple ex vivo method to generate large numbers of Foxp3-expressing iTregs that can be used to evaluate their trafficking properties, suppressive activity, and therapeu...
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PMID: 20941602
PDF is available here.
Abstract
We have used mice deficient in TNFSF member HVEM in experimental models of IBD to investigate its role in the disease process. Two models of IBD were employed: i) chemical-induced colitis primarily mediated by innate immune cells; and ii) colitis initiated by CD4(+)CD45RB(high) T cells following the...
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PMID: 21533159
PDF is available here.
Abstract
We developed a transgenic Lactobacillus acidophilus strain that constitutively expresses IFN-β (La-IFN-β). While pretreatment of mice with control Lactobacillus (La-EV) provided slight protective benefits, La-IFN-β increased sensitivity to DSS. Analysis showed colitic mice pretreated with La-IFN-...
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PMID: 21365015
PDF is available here.
Abstract
We conclude that E durans strain M4 to 5 and its metabolic product butyrate induce significant anti-inflammatory effects, mediated by regulation of pro- and anti-inflammatory immune factors as well as preservation of intestine epithelial integrity, suggesting that this novel anti-inflammatory bacter...
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PMID: 21178864
PDF is available here.
Abstract
We investigated the effect of PG extracted from salmon cartilage on the progression of experimental colitis-induced in severe combined immunodeficiency mice by cell transfer from interleukin-10 (IL-10)-/- mice. IL-10-/- cell-transferred mice showed weight loss, colon shortening and histological appe...
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PMID: 20969831
PDF is available here.
Abstract
We investigated, whether edible mushroom Pleurotus ostreatus (PO) has chemopreventive effect on inflammation-associated colon carcinogenesis induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and promoted by dextran sodium sulfate (DSS). PO treatment, at both doses (100 and 500 mg/kg)...
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PMID: 20878085
PDF is available here.
Abstract
Sophoridine (SRI), one of the quinolizidine alkaloids, is a new anticancer drug with noticeable antitumor action and lower toxicity. To our knowledge, there is no report about its effect on colitis. Repeated colitis was induced by administration of four cycles of 4% DSS. The severity of colitis was...
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PMID: 21061213
PDF is available here.
Abstract
We report three cases of NSAID colopathy in which the diagnosis of malignancy was incorrectly made based on endoscopic findings. Before any surgical intervention, we entertained the diagnosis of NSAID colopathy based on clinical presentation. Ultimately, in two of the three cases, surgery was avoide...
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PMID: 21140699
PDF is available here.
Abstract
To review evidence relating to the strength of associations that have appeared in largely observational studies, between high-dose or long-term use of proton pump inhibitor drugs and certain possibly attributable side-effects, which emerge from studies confounded by other variables. In retrospective...
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PMID: 20802330
PDF is available here.
Abstract
The specific purpose of this study was to evaluate the significant effects of medium-chain triglycerides (MCTs) and N-3 fatty acids on chemically induced experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid (TNBS) in rats. Male Wistar rats were fed liquid diets enrich...
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PMID: 20970751
PDF is available here.
Abstract
To investigate the effect of aqueous extract from Mangifera indica L. (MIE) on dextran sulfate sodium (DSS)-induced colitis in rats.
MIE (150 mg/kg) was administered in two different protocols: (1) rectally, over 7 d at the same time as DSS administration; and (2) once daily over 14 d (by oral gavag...
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PMID: 20954278
PDF is available here.
Keisuke Oboki,
Tatsukuni Ohno,
Naoki Kajiwara,
Ken Arae,
Hideaki Morita,
Akina Ishii,
Aya Nambu,
Takaya Abe,
Hiroshi Kiyonari,
Kenji Matsumoto,
Katsuko Sudo,
Ko Okumura,
Hirohisa Saito and
Susumu Nakae
Abstract
We found that IL-1, but not IL-33, played a substantial role in induction of T cell-mediated type IV hypersensitivity such as contact and delayed-type hypersensitivity and autoimmune diseases such as experimental autoimmune encephalomyelitis. Most notably, however, IL-33 was important for innate-typ...
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PMID: 20937871
PDF is available here.
Abstract
We hypothesized whether infliximab can prevent colitic cancer in animal models for which C57BL/6 mice were exposed to 15 cycles of dextran sulfate sodium (DSS), with each cycle consisting of 0.7% DSS for 1 week followed by sterilized water for 10 days. Infliximab (4 mg/kg i.v.) was given on the 1st,...
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PMID: 20736334
PDF is available here.
Abstract
We detected a strongly catecholaminergic character and in majority neuropeptide Y (NPY)-positive staining of the colon-projecting FB+ neurons both in the control and the inflamed animals. Furthermore, colonic inflammation caused the significant increase in density of galanin- (P<0.001), somatostatin...
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PMID: 20460841
PDF is available here.
Abstract
Collagenous gastritis, collagenous sprue, and collagenous colitis share striking histologic similarities and occur together in some patients. They also share some drug and disease associations. Pediatric cases of collagenous gastritis, however, lack most of these associations. The etiologies of the...
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PMID: 20923305
PDF is available here.
Abstract
We have used the complementary model of colonic inflammation to examine the roles of peroxisome proliferator-activated receptor α (PPARα) in colonic inflammation and thus its possible role in IBD. We characterized an innate immune-mediated model of colitis induced by dextran sulfate sodium (DSS)....
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PMID: 20650341
PDF is available here.
Abstract
We uncovered a novel role of OX40 in sustaining Treg competitive fitness in vivo, during repopulation of lymphopenic hosts and reconstitution of BM chimeras. Defective expansion of OX40-null Treg diminished their ability to suppress inflammation in a model of lymphopenia-driven colitis. OX40-mediate...
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PMID: 20806292
PDF is available here.
Sebastian E Winter,
Parameth Thiennimitr,
Maria G Winter,
Brian P Butler,
Douglas L Huseby,
Robert W Crawford,
Joseph M Russell,
Charles L Bevins,
L Garry Adams,
Renée M Tsolis,
John R Roth and
Andreas J Bäumler
Abstract
We show that reactive oxygen species generated during inflammation react with endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate. The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for...
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PMID: 20864996
PDF is available here.
Abstract
We focus on the most common and well-described drug-related clinico-pathological conditions of the gastrointestinal tract using an organ and lesion based approach....
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PMID: 20939398
PDF is available here.
Abstract
We demonstrated that T cell reactivity to IL-23 was critical for development of intestinal pathology, but not for systemic inflammation. Through direct signaling into T cells, IL-23 drove intestinal T cell proliferation, promoted intestinal Th17 cell accumulation, and enhanced the emergence of an IL...
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PMID: 20732640
PDF is available here.
Abstract
The NK-1R antagonist-treated animals had significantly reduced macroscopic and microscopic damage and decreased incidence of inflammatory bowel disease. Twice as many of these animals had a normal diagnosis in any region of the colon. A decrease in proliferation index, Cox-2 expression, and active E...
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PMID: 20944107
PDF is available here.
Abstract
A significant improvement was observed in DAI and histological score in rats with NPY antisense ODNs, and the increase in NPY and TNF-alpha levels, MPO activity, and the expression p-Akt and p-NF-kappaB in rats with DSS-induced colitis was significantly reduced following the administration of NPY an...
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PMID: 20533056
PDF is available here.
Abstract
We documented the anti-inflammatory effect of azithromycin in a murine model of acute colitis, suggesting that effects were targeted to oxidative burst and on mucosal/bacterial interface, independent of luminal bacterial load. Further studies should be focused on effect of azithromycin on the role o...
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PMID: 19924536
PDF is available here.
Abstract
We investigated whether omeprazole could prevent the development of colitis-associated cancer in a mouse model induced by repeated bouts of colitis. Omeprazole, 10 mg/kg, was given i.p. all through the experimental periods for colitis-associated carcinogenesis. Molecular changes regarding inflammati...
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PMID: 20628001
PDF is available here.
Markus M Heimesaat,
Axel Nogai,
Stefan Bereswill,
Rita Plickert,
André Fischer,
Christoph Loddenkemper,
Ulrich Steinhoff,
Sandrine Tchaptchet,
Eckhard Thiel,
Marina A Freudenberg,
Ulf B Göbel and
Lutz Uharek
Abstract
These results emphasise the critical role of gut microbiota, innate immunity and TLR9 in iGvHD and highlight anti-TLR9 strategies as novel therapeutic options....
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PMID: 20639251
PDF is available here.
Abstract
Ingestion of DSS solution can induce in rodents acute colitis with a massive infiltration of neutrophils and macropahges, mimicking pathological changes observed in the acute phase of UC patients. Concomitantly, DSS ingestion enhanced the expression of a potent macrophage-tropic chemokine, CX3CL1/fr...
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PMID: 20335311
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
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PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
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PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
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PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
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PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.
Abstract
We have reported that mice expressing a dominant negative form of transforming growth factor beta receptor II (dnTGFbetaRII) under control of the CD4 promoter develop both colitis and autoimmune cholangitis with elevated serum levels of IL-6. Based on this observation, we generated IL-6-deficient mi...
|
PMID: 20578264
PDF is available here.