• Title/Summary/Keyword: Inflammation bowel disease

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Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-$10^+F4/80^+$ Macrophage Recruitment

  • Jang, Sung-Won;Cho, Min-Kyoung;Park, Mi-Kyung;Kang, Shin-Ae;Na, Byoung-Kuk;Ahn, Soon-Cheol;Kim, Dong-Hee;Yu, Hak-Sun
    • Parasites, Hosts and Diseases
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    • v.49 no.3
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    • pp.245-254
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    • 2011
  • Many immune down-regulatory molecules have been isolated from parasites, including cystatin (cystain protease inhibitor). In a previous study, we isolated and characterized Type I cystatin (CsStefin-1) of the liver fluke, Clonorchis sinensis. To investigate whether the CsStefin-1 might be a new host immune modulator, we induced intestinal inflammation in mice by dextran sodium sulfate (DSS) and treated them with recombinant CsStefin-1 (rCsStefin-1). The disease activity index (DAI) increased in DSS only-treated mice. In contrast, the DAI value was significantly reduced in rCsStefin-1-treated mice than DSS only-treated mice. In addition, the colon length of DSS only-treated mice was shorter than that of rCsStefin-1 treated mice. The secretion levels of IFN-${\gamma}$ and TNF-${\alpha}$ in the spleen and mesenteric lymph nodes (MLNs) were significantly increased by DSS treatment, but the level of TNF-${\alpha}$ in MLNs was significantly decreased by rCsStefin-1 treatment. IL-10 production in both spleen and MLNs was significantly increased, and IL-$10^+F4/80^+$ macrophage cells were significantly increased in the spleen and MLNs of rCsStefin-1 treated mice after DSS treatment. In conclusion, rCsStefin-1 could reduce the intestinal inflammation occurring after DSS treatment, these effects might be related with recruitment of IL-10 secreting macrophages.

Effects of Moxi-tar Herbal Acupuncture of LI11 on inflammatory bowel disease induced by TNBS in mice (TNBS로 유도된 대장염에서 곡지의 구진약침 효과)

  • Song, Moon-Young;Park, Sang-Yeon;Kim, Jae-Hyo;Ahn, Sung-Hun;Kim, Kyoung-Sik;Sohn, In-Chul
    • Korean Journal of Acupuncture
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    • v.25 no.3
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    • pp.147-166
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    • 2008
  • Objectives : Crohn's disease (CD) is characterized by a chronic relapsing inflammation of the bowel in which proinflammatory cytokines play an important perpetuating role. Methods : Mice (preventive animal model of gliotoxin) were treated with 5 % 2,4,6-trinitrobenzenesulfonic acid (TNBS) at day 1 and day 7. To investigate preventive effects of acupuncture with Gujin at $LI_{11}$, acupuncture was carried out at day -1, day 1, day 3. And, to investigate therapeutic effects, acupuncture with Gujin was carried out at day 3, day 5, day 7. For the data analysis, we checked weight and width of colon, diarrhea, edema, survival rate, changes of body weight, and myeloperoxygenase (MPO) activity. For analysing protein expression, we carried out immunohistochemical staining and Western blot and we analyzed mRNA expression by RT-PCR. Results : Colon of TNBS treated mice was erosive and shortening compared with the colon of control mice and induced damages of colon epithelial cell layer and induced infiltration of immune cells in all layer of colon. Acupuncture of gujin at $LI_{11}$ in preventive mode suppressed macorscopic damages such as erosive and shortening of colon by TNBS and damages of intestinal epithelial cells and infiltration of immune cells in the colon. The average weight of 5 cm distal colon was increased in TNBS treated mice (758${\mu}g$) compared with in control mice (112${\mu}g$) and width of distal colon was also increased in TNBS treated mice (4.9mm) compared with in control mice (1.3mm). Acupuncture with Gujin at $LI_{11}$ in preventive and therapeutic mode suppressed increase of colon weight and width by TNBS. TNBS induced edema of colon and diarrhea and Acupunctured with Gujin at $LI_{11}$ in preventive and therapeutic mode ameliorated these symptom by TNBS. In preventive and therapeutic mode, the effects of acupuncture with Gujin at $LI_{11}$ were increasing the motility, suppressing body weight decreasing, suppressing MPO activity, reducing expressing of TNF-${\alpha}$, IL-1b, and ICAM-1 in colon compared with that by TNBS Conclusions : This study demonstrates that acupuncture with Gujin at $LI_{11}$ represents a potential therapeutic method of Crohn's disease.

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The Improving Effect of Gastrodia elata Blume on DSS-induced Colitis in Mice

  • Ahn, Eun-Mi;Kim, Su-Jin
    • Biomedical Science Letters
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    • v.24 no.3
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    • pp.168-174
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    • 2018
  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by abdominal pain, rectal bleeding and diarrhea. Gastrodia elata Blume (GE) has been used for the treatment of various diseases including neurodegenerative diseases and inflammatory disease. However, there has been no information on whether GE regulates intestinal inflammation. The aim of this study is to elucidate whether GE can protect against dextran sulfate sodium (DSS)-induced colitis in a mouse model. The colitis mice were induced by drinking water containing 5% DSS for 7 days. Body weight, colon length and clinical score were assessed to determine the effects on colitis. The levels of inflammatory cytokines, tumor necrosis factor $(TNF)-{\alpha}$ and interleukin (IL)-6 in colitis tissue were also measured. The results showed that mice administrated with DSS showed clinical signs including weight loss and reduced colon length. GE inhibited the DSS-induced loss of body weight and shortening of colon and increased Disease activity index score. Additionally, we observed that GE suppressed the levels of $TNF-{\alpha}$ and IL-6 in DSS-treated colon tissues. Collectively, these findings provide experimental evidence that GE might be a useful therapeutic agent for patients with UC.

Beneficial Effects of Riboflavin on Inflammatory Bowel Disease (리보플라빈의 염증성 장질환 개선 효과)

  • Sang Hee Lee;Sun Mi Hong;Mi Jeong Sung
    • Journal of the Korean Society of Food Culture
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    • v.39 no.1
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    • pp.74-81
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    • 2024
  • Ulcerative colitis (UC) is a chronic inflammatory intestinal disease characterized by an imbalance in immune function and the overexpression of inflammatory cytokines and mediators. Vitamin B2, also known as riboflavin (Libof), is an essential water-soluble vitamin with numerous beneficial properties, including antioxidant, anti-aging, anti-inflammatory, anti-nociceptive, and anti-cancer effects. In this study, we aimed to investigate the protective effects of Libof on dextran sulfate sodium (DSS)-induced experimental colitis. The C57BL/6 mice were used as the in vivo model of chronic colitis to investigate the anti-inflammatory effects of Libof. RAW 264.7 cells were used for the in vitro investigation of the molecular mechanisms underlying these effects. In vivo, Libof alleviated the DSS-induced disease activity index (DAI), colon length shortening, and colonic pathological damage. In vitro, Libof inhibited lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 production in RAW 264.7 cells. Moreover, Libof inhibited LPS-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in RAW 264.7 cells. In conclusion, these findings indicate that Libof shows potential as an agent for the treatment of UC.

Perspectives on the therapeutic potential of short-chain fatty acid receptors

  • Kim, Sunhong;Kim, Jeong-Hoon;Park, Bi Oh;Kwak, Young Shin
    • BMB Reports
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    • v.47 no.3
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    • pp.173-178
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    • 2014
  • There is rapidly growing interest in the human microbiome because of its implication in metabolic disorders and inflammatory diseases. Consequently, understanding the biology of short chain fatty acids and their receptors has become very important for identifying novel therapeutic avenues. GPR41 and GPR43 have been recognized as the cognate receptors for SCFAs and their roles in metabolism and inflammation have drawn much attention in recent years. GPR43 is highly expressed on immune cells and has been suggested to play a role in inflammatory diseases such as inflammatory bowel disease. Both GPR41 and GPR43 have been implicated in diabetes and obesity via the regulation of adipose tissue and gastrointestinal hormones. So far, many studies have provided contradictory results, and therefore further research is required to validate these receptors as drug targets. We will also discuss the synthetic modulators of GPR41 and GPR43 that are critical to understanding the functions of these receptors.

Interaction between Dietary Factors and Gut Microbiota in Ulcerative Colitis (궤양성 대장염에서 식이 인자와 장 마이크로비오타의 상호작용)

  • Mi-Kyung Sung
    • Journal of Digestive Cancer Research
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    • v.10 no.1
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    • pp.31-38
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    • 2022
  • Ulcerative colitis (UC) exhibits chronic intestinal inflammatory conditions with cycles of relapse and remission. The incidence is rapidly growing in Asian countries including South Korea possibly due to changes in lifestyles. Although the etiology of inflammatory bowel disease is inconclusive, gut microbiota composition is considered a critical factor involved in the pathogenesis of UC. The overgrowth of pathogenic bacteria evokes hyper-immune responses in gut epithelium causing tissue inflammation and damage. Also, failure to regulate gut epithelium integrity due to chronic inflammation and mucus depletion accelerates bacterial translocation aggravating immune dysregulation. Gut microbiota composition responds to the diet in a very rapid manner. Epidemiological studies have indicated that the risk of UC is associated with low plant foods/high animal foods consumption. Several bacterial strains consistently found depleted in UC patients use plant food-originated dietary fiber producing short chain fatty acids to maintain epithelial integrity. These bacteria also use mucus layer mucin to keep gut microbiota diversity. These studies partly explain the association between dietary modification of gut microbiota in UC development. Further human intervention trials are required to allow the use of specific bacterial strains in the management of UC.

Interferon-γ-mediated secretion of tryptophanyl-tRNA synthetases has a role in protection of human umbilical cord blood-derived mesenchymal stem cells against experimental colitis

  • Kang, Insung;Lee, Byung-Chul;Lee, Jin Young;Kim, Jae-Jun;Lee, Seung-Eun;Shin, Nari;Choi, Soon Won;Kang, Kyung-Sun
    • BMB Reports
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    • v.52 no.5
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    • pp.318-323
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    • 2019
  • Mesenchymal stem cells (MSCs) are multipotent adult stem cells that present immunosuppressive effects in experimental and clinical trials targeting various rare diseases including inflammatory bowel disease (IBD). In addition, recent studies have reported tryptophanyl-tRNA synthetase (WRS) possesses uncanonical roles such as angiostatic and anti-inflammatory effects. However, little is known about the function of WRS in MSC-based therapy. In this study, we investigated if a novel factor, WRS, secreted from MSCs has a role in amelioration of IBD symptoms and determined a specific mechanism underlying MSC therapy. Experimental colitis was induced by administration of 3% DSS solution to 8-week-old mice and human umbilical cord blood-derived MSCs (hUCB-MSCs) were injected intraperitoneally. Secretion of WRS from hUCB-MSCs and direct effect of WRS on isolated $CD4^+$ T cells was determined via in vitro experiments and hUCB-MSCs showed significant therapeutic rescue against experimental colitis. Importantly, WRS level in serum of colitis induced mice decreased and recovered by administration of MSCs. Through in vitro examination, WRS expression of hUCB-MSCs increased when cells were treated with interferon-${\gamma}$ ($IFN-{\gamma}$). WRS was evaluated and revealed to have a role in inhibiting activated T cells by inducing apoptosis. In summary, $IFN-{\gamma}$-mediated secretion of WRS from MSCs has a role in suppressive effect on excessive inflammation and disease progression of IBD and brings new highlights in the immunomodulatory potency of hUCB-MSCs.

Probiotics Inhibit Lipopolysaccharide-Induced Interleukin-8 Secretion from Intestinal Epithelial Cells

  • Oh, Hyun-Wook;Jeun, Gi-Hoon;Lee, Jin;Chun, Tae-Hoon;Kim, Sae-Hun
    • Food Science of Animal Resources
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    • v.32 no.4
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    • pp.434-440
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    • 2012
  • It has been suggested that probiotics could be useful for the prevention of symptomatic relapse in patients with inflammatory bowel disease (IBD). Interleukin (IL)-8 has been well recognized as one of the pro-inflammatory cytokines that could trigger inflammation and epithelial barrier dysfunction. In this study, the anti-inflammatory effects of probiotics were investigated using a human epithelial cell line (HT-29). Probiotics from infant feces and kimchi were tested for their cytotoxicity and effects on adhesion to epithelial cells. The present results show that seven strains could form 70 % adhesion on HT-29. The probiotics used in this study did not affect HT-29 cell viability. To screen anti-inflammatory lactic acid bacteria, HT-29 cells were pretreated with live and heat-killed probiotics, and lipopolysaccharide (LPS) ($1{\mu}g/mL$) was then added to stimulate the cells. The cell culture supernatant was then used to measure IL-8 secretion by ELISA, and the cell pellet was used to determine IL-8 and toll-like receptor (TLR-4) mRNA expression levels by RT-PCR. Some probiotics (KJP421, KDK411, SRK414, E4191, KY21, and KY210) exhibited anti-inflammatory effects through the repression of IL-8 secretion from HT-29 cells. In particular, Lactobacillus salivarius E4191, originating from Egyptian infant feces, not only decreased IL-8 mRNA expression, but also decreased TLR-4 expression. These results indicate that Lactobacillus salivarius E4191 may have a protective effect in intestinal epithelial cells.

Mechanisms of Motility Change on Trinitrobenzenesulfonic Acid-Induced Colonic Inflammation in Mice

  • Cheon, Gab Jin;Cui, Yuan;Yeon, Dong-Soo;Kwon, Seong-Chun;Park, Byong-Gon
    • The Korean Journal of Physiology and Pharmacology
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    • v.16 no.6
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    • pp.437-446
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    • 2012
  • Ulcerative colitis is an inflammatory bowel disease (IBD) characterized by recurrent episodes of colonic inflammation and tissue degeneration in human or animal models. The contractile force generated by the smooth muscle is significantly attenuated, resulting in altered motility leading to diarrhea or constipation in IBD. The aim of this study is to clarify the altered contractility of circular and longitudinal smooth muscle layers in proximal colon of trinitrobenzen sulfonic acid (TNBS)-induced colitis mouse. Colitis was induced by direct injection of TNBS (120 mg/kg, 50% ethanol) in proximal colon of ICR mouse using a 30 G needle anesthetized with ketamin (50 mg/kg), whereas animals in the control group were injected of 50% ethanol alone. In TNBS-induced colitis, the wall of the proximal colon is diffusely thickened with loss of haustration, and showed mucosal and mucular edema with inflammatory infiltration. The colonic inflammation is significantly induced the reduction of colonic contractile activity including spontaneous contractile activity, depolarization-induced contractility, and muscarinic acetylcholine receptor-mediated contractile response in circular muscle layer compared to the longitudinal muscle layer. The inward rectification of currents, especially, important to $Ca^{2+}$ and $Na^+$ influx-induced depolarization and contraction, was markedly reduced in the TNBS-induced colitis compared to the control. The muscarinic acetylcholine-mediated contractile responses were significantly attenuated in the circular and longitudinal smooth muscle strips induced by the reduction of membrane expression of canonical transient receptor potential (TRPC) channel isoforms from the proximal colon of the TNBS-induced colitis mouse than the control.

ent-Kaurane Diterpenoids from Croton tonkinensis Inhibit LPS-induced Transcription Factor NF-${\kappa}{B}$ Activation and NO Production

  • Giang, Phan-Minh;Jin, Hui-Zi;Lee, Jung-Joon
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.120.1-120.1
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    • 2003
  • Nuclear factor-${\kappa}{B}$ (NF-${\kappa}{B}$) belongs to a group of homodimers and heterodimers of Rel/NF-${\kappa}{B}$ proteins that bind to DNA target sites, where they directly regulate gene transcription. The activation of NF-${\kappa}{B}$ has been shown to mediate inflammation and suppress apoptosis. Activated NF-${\kappa}{B}$ has been found n various inflammatory diseases such as rheumatoid arthritis, Atherosclerosis, asthma, nflammatory bowel disease, and Helicobacter pylori-associated gastritis and associated with cancer, cachexia, diabetes, euthyroid sick syndrome, and AIDS. (omitted)

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