Correlation of neutrophil and monocyte derived interleukin-1 receptor antagonist and interleukin-8 with colitis severity in the rabbit

Kaneda, Kenta; Saitoh, Fumio; Shibusawa, Hirom; Maegawa, Hidetaka; Saniabadi, Abbi R.; Kashiwagi, Nobuhito; Matsukawa, Akihiro

doi:10.1016/j.cyto.2011.07.008

Cited by 7 publications

(10 citation statements)

References 27 publications

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“…In this model, TNBS can be administered without any anesthesia. A single dose of TNBS induces a reliable and reproducible model for colitis, showing similar macroscopic damage and histopathological changes in the colon as described previously [28–30, 35, 36]. …”

Section: Discussionsupporting

confidence: 69%

“…In rabbit, intrarectal instillation of TNBS also induced a typical colitis [28, 30, 35, 36]. After a single injection of TNBS (75 mg/kg), all animals reproducibly developed colitis with diarrhea and rectal bleeding to various extent as well as weight loss by 18.3 ± 4.7 % ( n = 8).…”

Section: Resultsmentioning

confidence: 99%

“…To elucidate the role of smooth muscle-derived immune/inflammatory response in intestinal disorders, we performed RT-qPCR array using the freshly isolated colonic circular smooth muscle strips. The ethanol treatment has been used as a vehicle control for TNBS-induced colitis as it does not induce dramatic histopathological changes in the colon [28, 30, 35, 36]. Most genes in this PCR array exhibited no significant changes between ethanol vehicle and normal control.…”

Section: Resultsmentioning

confidence: 99%

“…The action of NFκB signaling after colitis in mouse, rat, and human depends upon the induction of various immune/inflammatory responses [41]. In rabbit TNBS colitis model, IL-1β is significantly up-regulated [28, 29, 35]. IL-1β is known to regulate downstream target gene expression through classical and non-classical pathway of NFκB activation.…”

Section: Resultsmentioning

confidence: 99%

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Immune/Inflammatory Response and Hypocontractility of Rabbit Colonic Smooth Muscle After TNBS-Induced Colitis

Zhang

Wang

et al. 2016

Dig Dis Sci

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Background The contractility of colonic smooth muscle is dysregulated due to immune/inflammatory responses in inflammatory bowel diseases. Inflammation in vitro induces up-regulation of regulator of G-protein signaling 4 (RGS4) expression in colonic smooth muscle cells. Aims To characterize the immune/inflammatory responses and RGS4 expression pattern in colonic smooth muscle after induction of colitis. Methods Colitis was induced in rabbits by intrarectal instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Innate/adaptive immune response RT-qPCR array was performed using colonic circular muscle strips. At 1–9 weeks after colonic intramuscular microinjection of lentivirus, the distal and proximal colons were collected, and muscle strips and dispersed muscle cells were prepared from circular muscle layer. Expression levels of RGS4 and NFκB signaling components were determined by Western blot analysis. The biological consequences of RGS4 knockdown were assessed by measurement of muscle contraction and phospholipase C (PLC)-β activity in response to acetylcholine (ACh). Results Contraction in response to ACh was significantly inhibited in the inflamed colonic circular smooth muscle cells. RGS4, IL-1, IL-6, IL-8, CCL3, CD1D, and ITGB2 were significantly up-regulated, while IL-18, CXCR4, CD86, and C3 were significantly down-regulated in the inflamed muscle strips. RGS4 protein expression in the inflamed smooth muscles was dramatically increased. RGS4 stable knockdown in vivo augmented ACh-stimulated PLC-β activity and contraction in colonic smooth muscle cells. Conclusion Inflamed smooth muscle exhibits up-regulation of IL-1-related signaling components, Th1 cytokines and RGS4, and inhibition of contraction. Stable knockdown of endogenous RGS4 in colonic smooth muscle increases PLC-β activity and contractile responses.

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Section: Discussionsupporting

confidence: 69%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Immune/Inflammatory Response and Hypocontractility of Rabbit Colonic Smooth Muscle After TNBS-Induced Colitis

Zhang

Wang

et al. 2016

Dig Dis Sci

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“…The presence of eosinophils in the colonic mucosa has been associated with weight loss, malabsorption, changes in mucosal architecture, and reduced flattening of the villi and crypts in the colon . DSS‐induced colitis is also linked to the colonic migration of neutrophils, which triggers extensive tissue damage due to the release of free radicals . Accordingly, the reduction in colonic neutrophils is related to a better disease prognosis .…”

Section: Discussionmentioning

confidence: 99%

Systemic administration of a nanoemulsion with tributyrin reduces inflammation in experimental colitis

Leonel

Silva

Aguilar

et al. 2015

Euro J Lipid Sci & Tech

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Tributyrin (TBT) is a triacylglycerol formed by three molecules of butyrate that is able to improve colonic mucosal lesions and inflammation when given orally or as an enema. The effects of systemic TBT administration in inflammatory bowel disease (IBD) have been less well studied. We prepared a nanoemulsion containing tributyrin (nTBT) and studied its effects on a model of dextran sodium sulfate (DSS)-induced colitis. Mice were kept in the experiment for 15 days. Animals in the Colitis group received DSS (2.5% in their drinking water), whereas Control mice received only water during the last 7 experimental days. Animals were injected intraperitoneally (IP) with a nanoemulsion lacking TBT (Control and Colitis group) or containing TBT (Control nTBT and nTBT-Colitis) every other day for 15 days. Colonic mucosal damage and cytokine concentration were assessed by histopathological score and ELISA, respectively. Inflammatory infiltrates were assessed by enzymatic assay, and leukocyte rolling and adhesion in the colonic circulation were determined by intravital microscopy. Results revealed that the colonic architecture was not modified by nTBT administration. However, the colons of nTBT-Colitis mice presented reduced eosinophilic and neutrophilic infiltration associated with increased TGF-b concentrations compared to those of the Colitis group. Leukocyte rolling and adhesion were reduced in the nTBT-Colitis group, suggesting a systemic anti-inflammatory effect of nTBT. In conclusion, our results show that nTBT administered intraperitoneally is effective in reducing DSS-induced inflammation, whereas the trophic effects described with oral or local administration of TBT were not present when it was injected systemically.Practical applications: In this study, we show that the intraperitoneal administration of a nanoemulsion with tributyrin (nTBT) is able to reduce the inflammation observed in DSS-induced colitis. Due to its anti-inflationary actions, nTBT could be used in the future as a potential auxiliary drug in the treatment of inflammatory bowel diseases as well as other disorders with a systemic (low-grade) inflammatory component such as atherosclerosis and obesity.

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Myeloperoxidase (MPO): Do We Need Inhibitors?

Rajagopal

Narasimhulu

Khan

et al. 2017

Mechanisms of Vascular Defects in Diabetes Mellitus

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Correlation of neutrophil and monocyte derived interleukin-1 receptor antagonist and interleukin-8 with colitis severity in the rabbit

Cited by 7 publications

References 27 publications

Immune/Inflammatory Response and Hypocontractility of Rabbit Colonic Smooth Muscle After TNBS-Induced Colitis

Immune/Inflammatory Response and Hypocontractility of Rabbit Colonic Smooth Muscle After TNBS-Induced Colitis

Systemic administration of a nanoemulsion with tributyrin reduces inflammation in experimental colitis

Myeloperoxidase (MPO): Do We Need Inhibitors?

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