Effect of secondary lymphoid tissue chemokine suppression on experimental ulcerative colitis in mice

Zhang, H.; Zhang, X.; Ding, Xiaoling; Cao, Wei; Qu, Lei; Zhou, Guoqing

doi:10.4238/2014.april.29.12

Cited by 7 publications

(14 citation statements)

References 26 publications

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“…Li et al (2010) found that triptolide ameliorates colitis by suppressing the IL-6/signal transducer and activator of transcription 3 (STAT3) signaling pathway and downregulating IL-17. Zhang et al (2014) found that 0.6 mg/kg/day triptolide administration ameliorates intestinal injury by inhibiting the expression of secondary lymphoid tissue chemokine chemokine (C-C motif) ligand 21 (CCL21), which has chemotactic effects on T cells, B cells, NK cells, and DCs. However, they only investigated the expression of CCL21, which is not sufficient to demonstrate triptolide influence the chemotactic effects of T cells, B cells, NK cells, and DCs.…”

Section: Potential Effects Of Triptolide On Inflammatory Diseasesmentioning

confidence: 99%

Application and Mechanisms of Triptolide in the Treatment of Inflammatory Diseases—A Review

Yuan

et al. 2019

Front. Pharmacol.

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Bioactive compounds from medicinal plants with anti-inflammatory and immunosuppressive effects have been emerging as important sources of drugs for the treatment of inflammatory disorders. Triptolide, a diterpene triepoxide, is a pharmacologically active compound isolated from Tripterygium wilfordii Hook F (TwHF) that is used as a remedy for inflammatory and autoimmune diseases. As the most promising bioactive compound obtained from TwHF, triptolide has attracted considerable interest recently, especially for its potent anti-inflammatory and immunosuppressive activities. Over the past few years, an increasing number of studies have been published emphasizing the value of triptolide in the treatment of diverse inflammatory disorders. Here, we systematically review the mechanism of action and the therapeutic properties of triptolide in various inflammatory diseases according to different systematic organs, including lupus nephritis, inflammatory bowel disease, asthma, and rheumatoid arthritis with pubmed and Embase. Based on this review, potential research strategies might contribute to the clinical application of triptolide in the future.

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Section: Potential Effects Of Triptolide On Inflammatory Diseasesmentioning

confidence: 99%

Application and Mechanisms of Triptolide in the Treatment of Inflammatory Diseases—A Review

Yuan

et al. 2019

Front. Pharmacol.

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“…By comparing the effect of TL and dexamethasone on a mouse model of DSS-induced ulcerative colitis, the authors of the present study have previously indicated that TL may alleviate the symptoms of UC in the colons of mice by downregulating the expression of secondary lymphoid tissue chemokine, implying that TL may execute its therapeutic effect on UC by inhibiting the overexpression of secondary lymphoid tissue chemokine (37). …”

Section: Discussionmentioning

confidence: 77%

Therapeutic effects of triptolide via the inhibition of IL-1β expression in a mouse model of ulcerative colitis

Zhang

Chen

et al. 2016

Experimental and Therapeutic Medicine

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The present study aimed to investigate the effect of triptolide (TL) on ulcerative colitis (UC) and explore the potential association between the therapeutic effects of TL and IL-1β expression using a 4,4-dimethyl-4-silapentane-1-sulfonic acid (DSS)-induced mouse model to simulate human UC. A total of 70 BALB/c female mice were randomly allocated into seven equal groups: Group A, blank control; group B, normal saline injection; group C, propylene glycol injection; group D (TL1), 0.2 mg/kg TL; group E (TL2), 0.4 mg/kg TL; group F (TL3), 0.6 mg/kg TL; and group G, dexamethasone injection. Mice activity, diet and stool characteristics were recorded daily. Mice were sacrificed by cervical dislocation on day 8, and disease activity indices, colon tissue histological scores and colonic histopathological scores were subsequently calculated. Serum levels of IL-1β were evaluated by enzyme-linked immunosorbent assay, and IL-1β expression levels were examined by reverse transcription-quantitative polymerase chain reaction with colonic mucosa specimen at the gene level and western blot analysis at the protein level. The IL-1β mRNA and protein expression levels were significantly elevated in the normal saline injection and propylene glycol injection groups compared with the blank control group and (P<0.01). In TL (TL2 and TL3)- and dexamethasone-treated mice, IL-1β expression levels were significantly decreased, as compared with the normal saline and propylene glycol injection groups (P<0.05). No significant difference was detected between TL (TL2 and TL3) and dexamethasone treatments. The results of the present study indicated that IL-1β expression was upregulated in the UC mouse model, which may be associated with the development and progression of UC. Furthermore, TL inhibited IL-1β expression, suggesting that TL may be a novel therapeutic target for the treatment of UC.

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“…of inflammatory bowel diseases by selectively interfering with recruitment of naïve immune effector cells to sites of antigen presentation, without harming overall memory immunity [16][17][18][19].…”

Section: Plos Onementioning

confidence: 99%

“…While progress has been made, changing the natural history of inflammatory bowel diseases (IBD) is still problematic because the initiators of the disease are imperfectly defined [16,17]. The goal of interrupting the signaling cascade that leads to the destruction of the intestinal mucosa in these diseases has been hampered not just by the lack of targets but by the ineffectiveness of therapies against the targets that are known [5,8,[16][17][18][19]. Since the gut is its own secondary lymphoid organ where naïve lymphocytes can be presented antigen locally instead of maturing in a secondary lymphoid organ and then migrating to target inflamed/infected tissues, one potential IBD therapeutic target could be interrupting the migration of naïve lymphoid cells into the inflamed gut [5,7,8,16].…”

Section: Introductionmentioning

confidence: 99%

“…Since the gut is its own secondary lymphoid organ where naïve lymphocytes can be presented antigen locally instead of maturing in a secondary lymphoid organ and then migrating to target inflamed/infected tissues, one potential IBD therapeutic target could be interrupting the migration of naïve lymphoid cells into the inflamed gut [5,7,8,16]. CCL21 expression correlated with induction of ulcerative colitis in mice, and when that colitis was treated CCL21 expression decreased [8,18]. Therefore, we hypothesized that blocking CCL21-directed migration of naïve immune cells might alter the natural history of IBD [19,20].…”

Section: Introductionmentioning

confidence: 99%

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A humanized monoclonal antibody against the endothelial chemokine CCL21 for the diagnosis and treatment of inflammatory bowel disease

et al. 2021

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Chemokines are small proteins that promote leukocyte migration during development, infection, and inflammation. We and others isolated the unique chemokine CCL21, a potent chemo-attractant for naïve T-cells, naïve B-cells, and immature dendritic cells. CCL21 has a 37 amino acid carboxy terminal extension that is distinct from the rest of the chemokine family, which is thought to anchor it to venule endothelium where the amino terminus can interact with its cognate receptor, CCR7. We and others have reported that venule endothelium expressing CCL21 plays a crucial role in attracting naïve immune cells to sites of antigen presentation. In this study we generated a series of monoclonal antibodies to the amino terminus of CCL21 in an attempt to generate an antibody that blocked the interaction of CCL21 with its receptor CCR7. We found one humanized clone that blocked naïve T-cell migration towards CCL21, while memory effector T-cells were less affected. Using this monoclonal antibody, we also demonstrated that CCL21 is expressed in the mucosal venule endothelium of the large majority of inflammatory bowel diseases (IBD), including Crohn’s disease, ulcerative colitis, and also in celiac disease. This expression correlated with active IBD in 5 of 6 cases, whereas none of 6 normal bowel biopsies had CCL21 expression. This study raises the possibility that this monoclonal antibody could be used to diagnose initial or recurrent of IBD. Significantly, this antibody could also be used for therapeutic intervention in IBD by selectively interfering with recruitment of naïve immune effector cells to sites of antigen presentation, without harming overall memory immunity.

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Effect of secondary lymphoid tissue chemokine suppression on experimental ulcerative colitis in mice

Cited by 7 publications

References 26 publications

Application and Mechanisms of Triptolide in the Treatment of Inflammatory Diseases—A Review

Application and Mechanisms of Triptolide in the Treatment of Inflammatory Diseases—A Review

Therapeutic effects of triptolide via the inhibition of IL-1β expression in a mouse model of ulcerative colitis

A humanized monoclonal antibody against the endothelial chemokine CCL21 for the diagnosis and treatment of inflammatory bowel disease

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