15-deoxyspergualin prevents mucosal injury by inhibiting production of TNF-α and down-regulating expression of MD-1 in a murine model of TNBS-induced colitis

Lee, Jienny; Kim, Myung-Sunny; Kim, Eun Young; Park, Hae-Jung; Chang, Chi Young; Jung, Da-Yeon; Kwon, Choon Hyuck David; Joh, Jae‐Won; Kim, Jong Man

doi:10.1016/j.intimp.2007.02.015

Cited by 9 publications

(7 citation statements)

References 58 publications

(51 reference statements)

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“…Whereas this study showed no significant decrease in the TNF-α levels by MSCs, Lee et al. (29,30) showed that DSG and anti-4-1 BB mAb leads to a decrease in TNF-α levels. However, TNF-α significantly increased only on day 3 but not on day 10 in this study, which can be interpreted as MSCs working more effectively in the later part of the inflammation process and not in the earlier part.…”

Section: Discussioncontrasting

confidence: 70%

Immunomodulatory Effects of Mesenchymal Stem Cells in a Murine Model of TNBS-Induced Colitis

et al. 2010

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Section: Discussioncontrasting

confidence: 70%

Immunomodulatory Effects of Mesenchymal Stem Cells in a Murine Model of TNBS-Induced Colitis

et al. 2010

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“…Under physiologic conditions the mucosa is constantly exposed to external surroundings abundant in foreign antigens (e.g., bacterial); the reservoir of B cells in this layer is necessary for production of antibodies needed to protect against pathogens. TNBS insult results not only in the accumulation of antigen-like molecules in the colon but also disrupts its mucosal barrier; thus, the recruitment and/or proliferation of B cells is observed in the deeper, submucosal layer of the colonic tissue (Lee et al, 2007). Treatment with encenicline significantly reduced the number of B cells present in the colon.…”

Section: Encenicline In Colitismentioning

confidence: 99%

Encenicline, an 7 Nicotinic Acetylcholine Receptor Partial Agonist, Reduces Immune Cell Infiltration in the Colon and Improves Experimental Colitis in Mice

Sałaga

Blomster

Piechota-Polańczyk³

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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The a7 pentamer nicotinic acetylcholine receptors (nAChRs) are a target in transduction of anti-inflammatory signals from the central nervous system to the gastrointestinal (GI) tract. The aim of this study was to investigate the anti-inflammatory action of the novel a7 nAChR partial agonist encenicline and to determine the mechanism underlying its activity. Anti-inflammatory activity of encenicline was evaluated using trinitrobenzenesulfonic acid (TNBS)-and dextran sulfate sodium (DSS)-induced models of colitis. Macroscopic score, ulcer score, colon length and thickness, as well as myeloperoxidase (MPO) activity were recorded. Immunohistochemistry (IHC) was used to measure the infiltration of immune cells in the colon. Furthermore, we employed flow cytometry to determine the effect of encenicline on frequencies of FoxP3 1 and interleukin (IL)-17A 1 T cells in the mouse colon. Encenicline attenuated TNBS-and DSS-induced colitis in mice via a7 nAChRs, as indicated by significantly reduced macroscopic parameters and MPO activity. Treatment with encenicline significantly reduced the infiltration of macrophages, neutrophils, and B cells in the colon of TNBS-treated animals, as indicated by IHC. In the TNBS model encenicline reduced the frequency of FoxP3

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“…Among them, tumor necrosis factor alpha (TNF-α) is abundantly present in the serum of IBD patients [38] and is highly expressed in the gut of animal models of TNBS-induced colitis [14,28,43]. Moreover, several studies demonstrated that TNF-α impairs the contractility of arterial vessels [7,8,78].…”

Section: Introductionmentioning

confidence: 99%

“…9 Among them, TNFα is abundantly present in the serum of patients with IBD 10 and is highly expressed in the gut of animal models of TNBS-induced colitis. [11][12][13] Moreover, several studies demonstrated that TNFα impairs the contractility of arterial vessels. [14][15][16] Based on these findings, we explored the possibility that TNFα might also alter the contractile ability of lymphatic vessels and hypothesized that dysfunctional lymphatic pumping we demonstrated in model of TNBS-induced ileitis 1,2 is possibly due to the increased, inflammation-induced production of TNFα and its detrimental action on mesenteric lymphatic vessels.…”

mentioning

confidence: 99%

The pro‐inflammatory cytokineTNF‐α inhibits lymphatic pumping via activation of theNF‐κB‐iNOSsignaling pathway

et al. 2017

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Objective Mesenteric lymphatic vessels pumping, important to propel lymph and immune cells from the intestinal interstitium to the mesenteric lymph nodes, is compromised during intestinal inflammation. The objective of this study was to test the hypothesis that the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α), is a significant contributor to the inflammation-induced lymphatic contractile dysfunction, and to determine its mode of action. Methods Contractile parameters were obtained form isolated rat mesenteric lymphatic vessels mounted on a pressure myograph after 24-h incubation with or without TNF-α. Various inhibitors were administered and quantitative real-time PCR, western blotting and immunofluorescence confocal imaging were applied to characterize the mechanisms involved in TNF-α actions. Results Vessel contraction frequency was significantly decreased after TNF-α treatment and could be restored by selective inhibition of NF-кB, iNOS, guanylate cyclase and ATP-sensitive K+ channels. We further demonstrated that NF-кB inhibition also suppressed the significant increase in iNOS mRNA observed in TNF-α-treated lymphatic vessels and that TNF-α treatment favor the nuclear translocation of the p65 NF-κB subunit. Conclusions These findings suggest that TNF-α decreases mesenteric lymphatic contractility by activating the NF-κB - iNOS signaling pathway. This mechanism could contribute to the alteration of lymphatic pumping reported in intestinal inflammation.

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15-deoxyspergualin prevents mucosal injury by inhibiting production of TNF-α and down-regulating expression of MD-1 in a murine model of TNBS-induced colitis

Cited by 9 publications

References 58 publications

Immunomodulatory Effects of Mesenchymal Stem Cells in a Murine Model of TNBS-Induced Colitis

Immunomodulatory Effects of Mesenchymal Stem Cells in a Murine Model of TNBS-Induced Colitis

Encenicline, an 7 Nicotinic Acetylcholine Receptor Partial Agonist, Reduces Immune Cell Infiltration in the Colon and Improves Experimental Colitis in Mice

The pro‐inflammatory cytokineTNF‐α inhibits lymphatic pumping via activation of theNF‐κB‐iNOSsignaling pathway

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