Exosomes derived from interleukin-10-treated dendritic cells can inhibit trinitrobenzene sulfonic acid-induced rat colitis

Yang, Xiaojun; Shao, Meng; Jiang, Hong; Chen, Tao; Wu, Wei

doi:10.3109/00365521.2010.490596

Cited by 70 publications

(63 citation statements)

References 28 publications

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“…Thus, it is possible that observed amelioration of the disease in our system after skin patching with TNP-Ig is partly mediated by IL-10. Our finding is in line with report from other laboratories showing that indeed IL-10 plays an important role in controlling inflammatory response during TNBS-colitis [4,28]. However, other sources of these cytokine are possible.…”

Section: Discussionsupporting

confidence: 93%

Epicutaneous immunization with protein antigen TNP-Ig alleviates TNBS-induced colitis in mice

Majewska‐Szczepanik

Góralska

Marcińska

et al. 2012

Pharmacological Reports

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Abstract:Background: Ulcerative colitis (UC) is a chronic inflammatory autoimmune disease with limited treatment modalities. The animal model of colitis induced by treatment with trinitrobenzene sulfonic acid (TNBS-colitis) is commonly used to test new therapies of this disease. In our previous work we found that epicutaneous (EC) immunization with protein antigen induced a state of profound immunosuppression that inhibited inflammatory response in contact sensitivity, in experimental autoimmune encephalomyelitis (EAE) and in allogeneic skin graft rejection. Methods: TNBS-induced colitis was used as an experimental model. Results: In our current work, we showed that EC immunization with TNP-conjugated mouse immunoglobulin (TNP-Ig) prior to induction of TNBS-colitis alleviates disease severity what was determined by the body weight, the length and the weight of the colon, the histological activity index (HAI) and myeloperoxidase activity (MPO). Observed amelioration of the disease in TNP-Ig patched mice was accompanied with decreased production of IFN-g and IL-17A by splenocytes. Additionally, spleen cells isolated from mice EC immunized with TNP-Ig prior to colitis induction showed increased production of IL-10 suggesting that this cytokine might be involved in inhibiting inflammatory response in the colon. Conclusion: This work shows that EC immunization with protein antigen prior to TNBS-colitis induction ameliorates disease and observed suppression of inflammatory response in the colon might be mediated by IL-10.

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Section: Discussionsupporting

confidence: 93%

Epicutaneous immunization with protein antigen TNP-Ig alleviates TNBS-induced colitis in mice

Majewska‐Szczepanik

Góralska

Marcińska

et al. 2012

Pharmacological Reports

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“…IL-10 concentration increased 2.4-fold times when compared to that of colitic mice. Since IL-10 itself functions as an anti-inflammatory cytokine and limits excessive tissue disruption caused by inflammation [29,30], our findings suggest that the anti-inflammatory effect of TDZD-8 is due not only to suppression of TNF-α and IL-1β but also to increase of IL-10 production. …”

Section: Discussionmentioning

confidence: 69%

Thiadiazolidinone-8 Ameliorates Inflammation Associated with Experimental Colitis in Mice

et al. 2017

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Thiadiazolidinone-8 (TDZD-8) is an effective thiadiazolidinone derivate that is able to suppress the expression of inflammatory cytokines; it also presents tissue protective actions by glycogen synthase kinase (GSK)-3β inhibition, promoting thus an anti-inflammatory effect. Since inflammatory bowel disease is a chronic disease with reduced quality of life, where currently available therapies are only able to induce or maintain the patient in remission, it is crucial to investigate new pharmacological approaches. The main objective of this study was to evaluate the effect of TDZD-8 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Male CD-1 mice with TNBS-induced colitis were treated with a daily dose of TDZD-8 5 mg/kg/day IP during 4 days. The anti-inflammatory properties of TDZD-8 in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and myeloperoxidase, as well as by the significant increase of the anti-inflammatory cytokine, IL-10. These treated mice also presented a reduction in fecal hemoglobin and alkaline phosphatase, suggesting a beneficial effect of TDZD-8. Furthermore, renal and hepatic biomarkers remained stabilized after treatment. In conclusion, TDZD-8 reduces the inflammatory response associated with TNBS-induced colitis in mice, and modulation of GSK-3β seems to be an interesting pharmacological target in colitis.

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“…Also membrane-associated IL-10 and IL-4 have been demonstrated on vesicles under certain circumstances. DC incubated with IL-10 or modified to express membrane-bound IL-4 release vesicles with respectively membrane-associated IL-10 or IL-4 [123,124]. These vesicles appeared to have an immune suppressive effect.…”

Section: Cell-derived Vesicles As Carriers For Cytokines and Cytokinementioning

confidence: 82%

“…These vesicles appeared to have an immune suppressive effect. The IL-10 containing vesicles tend to skew T cell responses away from effector T cell responses toward regulatory T cell responses [123], while the IL-4/DC derived vesicles efficiently inhibited delayed type hypersensitivity (DTH) responses [124].…”

Section: Cell-derived Vesicles As Carriers For Cytokines and Cytokinementioning

confidence: 99%

Immune Cell-derived Vesicles: Modulators and Mediators of Inflammation

Hoen¹,

Wauben

2012

CPD

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Most cell types can release vesicles. Cell-derived vesicles are increasingly recognized as an evolutionary wide-spread mechanism of intercellular communication. The paracrine and long range activity of vesicles and their regulated cargo-composition endows these vesicles with regulatory properties beyond that of the parental cell. The release and biogenesis of cell-derived vesicles is a dynamic and tightly controlled process. In the past years it has become clear that these vesicles exert a plethora of biological effects. This has sparked the intense interest in these vesicles in relation to (patho)physiological processes. This review focuses on the role of cell-derived vesicles in inflammation, with emphasis on the immune modulating capacity of immune cell-derived vesicles. The biological activity of different leukocyte-derived vesicles is compared, and potential explanations for the strong biological effects exhibited by vesicles are provided. The role of cell-derived vesicles in inflammatory processes is discussed by speculating how these vesicles can contribute to allergic inflammation.

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Exosomes derived from interleukin-10-treated dendritic cells can inhibit trinitrobenzene sulfonic acid-induced rat colitis

Abstract: The results suggest that IL-10-exosomes treatment can suppress acute TNBS-induced colitis and may offer a promising new therapeutic strategy for IBD.

Cited by 70 publications

References 28 publications

Epicutaneous immunization with protein antigen TNP-Ig alleviates TNBS-induced colitis in mice

Epicutaneous immunization with protein antigen TNP-Ig alleviates TNBS-induced colitis in mice

Thiadiazolidinone-8 Ameliorates Inflammation Associated with Experimental Colitis in Mice

Immune Cell-derived Vesicles: Modulators and Mediators of Inflammation

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