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Objectives: Inflammatory cytokine secretion and gut microbiota dysbiosis play crucial roles in ulcerative colitis. In this research, the protective effects of peimisine on colitis mice were investigated. Methods: The protective effects were evaluated by the disease activity index, colonic length, hematoxylin–eosin, and AB/PAS Staining. The protective mechanisms were analyzed by ELISA, Western-blot, immunohistochemistry staining, immunofluorescence staining, and 16S rRNA gene analysis. Key findings: The results showed that peimisine treatment could reduce the disease activity index, prevent colonic shortening, and alleviate colon tissue damage. Peimisine treatment also decreased the levels of MCP-1, IL-1β, IL-6, IFN-γ, TNF-α and affected macrophage polarization and Th17/Treg cell balance by downregulating the expression of jak1/2, p-jak1/2, stat1/3, and p-stat1/3. Moreover, peimisine treatment significantly increased the abundances of beneficial microbes (e.g. Ruminococcaceae UCG-014 and Lachnospiraceae_NK4A136_group) and decreased the abundances of harmful microbes (e.g. Bacteroides and Escherichia). Conclusions: Peimisine can ameliorate colitis by inhibiting Jak–Stat signaling pathway, reversing gut microbiota alterations, suppressing macrophage M1 polarization, maintaining the Th17/Treg cell balance, and reducing sustained inflammatory cytokines-related inflammatory injury. [ABSTRACT FROM AUTHOR]

Abstract Background Intestinal inflammation has become a threatening concern in chicken production worldwide and is closely associated with Th17/Treg cell imbalance. Several studies described that gut microbiota is significantly implicated in chicken growth by modulating intestinal immune homeostasis and immune cell differentiation. Whether reshaping gut microbiota by fecal microbiota transplantation (FMT) could improve chicken growth by balancing Th17/Treg cells is an interesting question. Results Here, the chickens with significantly different body weight from three different breeds (Turpan cockfighting × White Leghorn chickens, white feather chickens, and yellow feather chickens) were used to compare Th17 and Treg cells. qPCR and IHC staining results indicated that Th17 cell-associated transcriptional factors Stat3 and rorγt and cytokines IL-6, IL-17A, and IL-21 were significantly (P

Chronic inflammation plays a critical role in the pathogenesis of postmenopausal osteoporosis (PMO). Short-chain fatty acids (SCFAs) produced by the gut microbiota (GM) have emerged as key regulators of the inflammatory response. Cistanche deserticola polysaccharide (CDP), derived from the traditional Chinese medicine Cistanche deserticola, possesses potent anti-inflammatory properties. However, the precise mechanism by which CDP modulates inflammation in PMO via the gut-bone axis remains elusive. In this study, we elucidated that CDP could effectively restore GM composition, ameliorate intestinal mucosal damage, elevate SCFA levels, rebalance the Th17/Treg cells equilibrium, attenuate the accumulation of proinflammatory cytokines, potentially facilitate osteoblast differentiation, potentially suppress osteoclastogenesis, and enhance bone microarchitecture in PMO mice. Collectively, our findings provided compelling evidence that CDP alleviated PMO-associated inflammation, potentially mediated through the intricate interplay between GM-derived SCFAs and the Th17/Treg cells.

Background: Intestinal inflammation has become a threatening concern in chicken production worldwide and is closely associated with Th17/Treg cell imbalance. Several studies described that gut microbiota is significantly implicated in chicken growth by modulating intestinal immune homeostasis and immune cell differentiation. Whether reshaping gut microbiota by fecal microbiota transplantation (FMT) could improve chicken growth by balancing Th17/Treg cells is an interesting question. Results: Here, the chickens with significantly different body weight from three different breeds (Turpan cockfighting × White Leghorn chickens, white feather chickens, and yellow feather chickens) were used to compare Th17 and Treg cells. qPCR and IHC staining results indicated that Th17 cell-associated transcriptional factors Stat3 and rorγt and cytokines IL-6, IL-17A, and IL-21 were significantly (P < 0.05) higher in the jejunum of low body weight chickens, while Treg cell-associated transcriptional factor foxp3 and cytokines TGF-β and IL-10 were significantly (P < 0.05) lower in the jejunum of low body weight chickens, indicating imbalanced Th17/Treg cells were closely related to chicken growth performance. Transferring fecal microbiota from the healthy donor with better growth performance and abundant Lactobacillus in feces to 1-day-old chicks markedly increased growth performance (P < 0.001), significantly decreased Th17 cell-associated transcriptional factors and cytokines, and increased Treg cell-associated transcriptional factors and cytokines in the jejunum (P < 0.05). Furthermore, FMT increased the abundance of Lactobacillus (FMT vs Con; 84.98% vs 66.94%). Besides, the metabolites of tryptophan including serotonin, indole, and 5-methoxyindoleacetate were increased as well, which activated their receptor aryl-hydrocarbon-receptor (AhR) and expressed more CYP1A2 and IL-22 to maintain Th17/Treg cell balance and immune homeostasis. Conclusion: These findings suggested that imbalanced Th17/Treg cells decreased chicken growth performance, while FMT-reshaped gut microbiota, i.e., higher Lactobacilli, increased chicken growth performance by balancing Th17/Treg cells. Bkgy_kqRX8WcaCpUPJnFa8 Video Abstract [ABSTRACT FROM AUTHOR]

The imbalance of Th17 and Treg cell differentiation, intestinal flora imbalance, and intestinal mucosal barrier damage may be important links in the occurrence and development of inflammatory bowel disease (IBD) since Th17 and Treg differentiation are affected by the intestinal flora. This study aimed to explore the effect of Escherichia coli (E. coli) LF82 on the differentiation of Th17 and Treg cells and the role of the intestinal flora in mouse colitis. The effects of E. coli LF82 infection on intestinal inflammation were evaluated by analyzing the disease activity index, histology, myeloperoxidase activity, FITC-D fluorescence value, and claudin-1 and ZO-1 expression. The effects of E. coli LF82 on the Th17/Treg balance and intestinal flora were analyzed by flow cytometry and 16S rDNA sequencing. Inflammatory markers, changes in the intestinal flora, and Th17/Treg cells were then detected after transplanting fecal bacteria from normal mice into colitis mice infected by E. coli LF82. We found that E. coli LF82 infection can aggravate the intestinal inflammation of mice colitis, destroy their intestinal mucosal barrier, increase intestinal mucosal permeability, and aggravate the imbalance of Th17/Treg differentiation and the disorder of intestinal flora. After improving the intestinal flora imbalance by fecal bacteria transplantation, intestinal inflammation and intestinal mucosal barrier damage were reduced, and the differentiation balance of Th17 and Treg cells was restored. This study showed that E. coli LF82 infection aggravates intestinal inflammation and intestinal mucosal barrier damage in colitis by affecting the intestinal flora composition and indirectly regulating the Th17 and Treg cell differentiation balance. [ABSTRACT FROM AUTHOR]

Psoriasis is a chronic papulosquamous skin disease occurring worldwide caused by varieties of factors. The recipe of Mongolian medicine Sendeng Decoction was recorded in “The Pleasure of the Viewer” compiled by Jigwood Danjinzhamusu. Mongolian medicine clinical experience proved that Sendeng Decoction had good antipyretic, analgesic, anti-inflammatory and anti-rheumatism effect. However, the mechanism of this drug in psoriasis is still unclear. In this study, imiquimod cream (IMQ) was used to construct psoriasis model in 8-week-old male BALB/c mice, and Sendeng Decoction was used to treat the mice with psoriasis. The results showed that PASI score and spleen index decreased after Sendeng Decoction treatment. Meanwhile, HE staining showed that the pathological structure was improved, flow cytometry results showed that the proportion of Treg cells increased and Th17 ​cells decreased, and results of Western blot showed that the level of p38 MAPK, p-p38 MAPK, p-STAT3 and p-JAK1 decreased observably. More importantly, the above results were most significant in Sendeng's M group, which was similar to MTX group. Our results indicated that Mongolian medicine Sendeng Decoction can effectively relieve the symptoms of psoriasis mice induced by IMQ, mainly by regulating the ratio of Th17/Treg cells through the JAK/STAT and p38 MAPK pathways to reduce the inflammatory state in mice, thereby improving the symptoms of dermatitis.

Atractylodes macrocephala Koidz. is one of the most frequently used traditional Chinese medicines for the treatment of ulcerative colitis (UC). The beneficial effect of polysaccharide from Atractylodes macrocephala Koidz. (PAMK) on UC has been reported, while the underlyingmechanism and target remain unclear. In this study, we systematically investigated the therapeutic effect and the underlying mechanism of PAMK in UC based on a mouse model of dextran sodium sulfate (DSS)-induced colitis. PAMK treatment (100 mg/kg, 200 mg/kg and 400 mg/kg) significantly ameliorated DSS-induced colitis, manifested as a reduction in weight loss, disease activity index (DAI), colon shortening, spleen index and histological score. Moreover, PAMK treatment inhibited inflammation and improved the integrity of the intestinal barrier in colitis mice. Mechanistically, microarray analysis determined the critical role of the immunoregulatory effect of PAMK in alleviating UC. Flow cytometry analysis further demonstrated that PAMK treatment regulated the balance between T helper (Th) 17 and regulatory T (Treg) cells in the mesenteric lymph nodes (MLN) and spleen in mice with colitis. In addition, PAMK treatment downregulated the expression of IL-6 and suppressed the phosphorylation of STAT3. Together, these data revealed that PAMK treatment alleviated DSS-induced colitis by regulating the Th17/Treg cell balance, which may be dependent on the inhibition of the IL-6/STAT3 signaling pathway. Our study is the first to elucidate that the underlying mechanism by which PAMK treatment alleviates DSS-induced colitis is associated with an improved the Th17/Treg cell balance. Collectively, the study provides evidence for the potential of PAMK to treat UC. [ABSTRACT FROM AUTHOR]

Li Li,1,2,&ast; Wenqi Shan,1,3,&ast; Haijin Zhu,1,3,&ast; Fei Xue,1,2 Yongbin Ma,1,4 Liyang Dong,1,5 Dingqi Feng,1 Jiahui Mao,1 Guoyue Yuan,6 Xuefeng Wang1,5 1Department of Central Laboratory, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, People’s Republic of China; 2Department of Clinical Laboratory, The Taixing City People’s Hospital, Taixing, 225400, People’s Republic of China; 3Department of Pediatrics, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, People’s Republic of China; 4Department of Central Laboratory, Jintan Hospital, Jiangsu University, Jintan, 213200, People’s Republic of China; 5Department of Nuclear Medicine and Institute of Oncology, The Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, People’s Republic of China; 6Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, 212001, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Xuefeng Wang; Liyang DongDepartment of Central Laboratory, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang, 212001, People’s Republic of ChinaTel +86-511-8502-1135; +86-511-8502-6569Email xuefengwang@ujs.edu.cn; dongliyang0829@hotmail.comPurpose: Helminths and their products can regulate immune response and offer new strategies to control and alleviate inflammation, including asthma. We previously found that a peptide named as SJMHE1 from Schistosoma japonicum can suppress asthma in mice. This study mainly investigated the molecular mechanism of SJMHE1 in inhibiting asthma inflammation.Methods: SJMHE1 was administered to mice with OVA-induced asthma via subcutaneous injection, and its effects were detected by testing the airway inflammation of mice. The Th cell distribution was analyzed by flow cytometry. Th-related transcription factor and cytokine expression in the lungs of mice were analyzed using quantitative real-time PCR (qRT-PCR). The expression of miR-155 and levels of phosphorylated STAT3 and STAT5 were also determined after SJMHE1 treatment in mice by qRT-PCR and Western blot analysis. The in vitro mouse CD4+ T cells were transfected with lentivirus containing overexpressed or inhibited miR-155, and the proportion of Th17, Treg cells, CD4+p-STAT3+, and CD4+p-STAT5+ cells were analyzed by flow cytometry.Results: SJMHE1 ameliorated the airway inflammation of asthmatic mice, upregulated the proportion of Th1 and Treg cells, and the expression of Th1 and Treg-related transcription factor and cytokines. Simultaneously, SJMHE1 treatment reduced the percentage of Th2 and Th17 cells and the expression of Th2 and Th17-related transcription factor and cytokines. SJMHE1 treatment decreased the expression of miR-155 and p-STAT3 but increased p-STAT5 expression. In vitro, the percentage of Th17 and CD4+p-STAT3+ cells increased in CD4+ T cells transfected over-expression of miR-155, but SJMHE1 inhibited the miR-155-mediated increase of Th17 cells. Furthermore, SJMHE1 increased the proportion of Treg and CD4+p-STAT5+ cells after transfected over-expression or inhibition of miR-155.Conclusion: SJMHE1 regulated the balance of Th17 and Treg cells by modulating the activation of STAT3 and STAT5 via miR-155 in asthma. SJMHE1 might be a promising treatment for asthma.Keywords: Schistosoma japonicum peptide, SJMHE1, Th17/Treg cell balance, miR-155, asthma

Objective: Compound sophorae decoction, a Chinese medicinal formulae composed of six Chinese herbs, is effective for the clinical treatment of ulcerative colitis (UC). Some of its effective monomers had been proven to have suppressive effect on UC models. The aim of this study is to further explore the mechanism whether compound sophorae decoction ameliorates dextran sodium sulfate (DSS)-induced mice colitis by regulating the balance between T helper (Th) 17 and regulatory T (Treg) cells. Methods: Experimental model of UC, established by drinking water with DSS, was treated with compound sophorae decoction and mesalazine. The stool, activity, body weight of the mice, colon length and colon histopathology were observed to evaluate severity of colitis. The concentration of cytokines in colonic tissues were detected by ELISA. The expression of phosphorylated nuclear factor-kappaB (NF-κB) p65, STAT3 and phosphorylated STAT3 in colonic tissues were determined by western blotting and immunohistochemistry. The percentage of Th17 and Treg cells in spleen and mesenteric lymph nodes (MLNs) were detected by flow cytometry. The levels of transcription factor ROR-γt and FOXP3 in colon tissues were detected by qRT-PCR and immunohistochemistry. Results: The aqueous extract of compound sophorae decoction was able to improve the symptoms and pathological damage of mice. The body weight of mice were increased and DAI were significantly decreased; ulcers were slighter than DSS group. The administration of compound sophorae decoction reduced the level of inflammatory factors interleukin (IL)-1β, tumor necrosis factor (TNF)-α and phospho-NF-κB p65, and also decreased the proportions of Th17 cells in spleen and MLNs and the expression of ROR-γt, IL-17A, STAT3, IL-6 in colonic tissues; while the percentage of Treg cells in spleen and MLNs and the expression of FOXP3, transforming growth factor (TGF)-β1, IL-10 in colonic tissues were upregulated. Conclusion: Overall, this study suggested that compound sophorae decoction significantly improves the symptoms and the pathological damage of mice with colitis and influences the immune function by regulating Th17/Treg cell balance in DSS-induced colitis in mice.

Background: Th subsets particularly T helper 17 and regulatory T cells play a critical role in immune balance in colonic mucosa of Inflammatory Bowel Disease. Recent studies have indicated miR-155 is overexpressed in the colonic mucosa in IBD patients. Thus, whether and how miR-155 influences Th17/Treg cell balance in IBD patients is worthy of researching. Methods: We divided mice into four groups: the mice oral administration of 3.0 % DSS in fresh drinking water for 7 days except normal group. In this period, starting from the fifth day, the miR-155 and NC antagomir group were carried out by intraperitoneal injection of miR-155 antagomirs and corresponding negative controls. In vitro, we isolated naïve CD4+T cells and divided into two groups: the cells were transfected with mmu-miR-155-5p inhibitor or corresponding negative controls and then induced differentiation. Results: We found miR-155 antagomir can reach colon tissues in DSS-induced colitis and indeed ameliorated DSS-induced experimental colitis. Subsequently, we proved the levels of Th17 cells in spleens and Mesenteric lymph nodes and its associated IL-6, IL-17A and RORγt in colonic tissues were dramatically decreased and TGF-β1 raised in DSS + miR-155 antagomir group. However, miR-155 antagomir significantly increased the expression of Tregs. In vitro, we found miR-155 inhibitor could improve the Tregs but decrease Th17 cells. Finally, we dig out that Jarid2 was apparently improved by miR-155 antagomir, Wnt/β-catenin and its associated T cell factor-4 (TCF-4) and Cyclin D1 expression were positively correlated with Jarid2. Conclusion: Silencing of miR-155 attenuates DSS-induced colitis by regulating Th17/Treg cell balance and Jarid2/Wnt/β-catenin participated in the process.

Highlights • Compound sophorae decoction is effective for the treatment of UC. • Compound sophorae decoction ameliorates symptoms in DSS-induced mice colitis. • Compound sophorae decoction regulates the balance between Th17 and Treg cells in the UC mouse model. Abstract Objective Compound sophorae decoction, a Chinese medicinal formulae composed of six Chinese herbs, is effective for the clinical treatment of ulcerative colitis (UC). Some of its effective monomers had been proven to have suppressive effect on UC models. The aim of this study is to further explore the mechanism whether compound sophorae decoction ameliorates dextran sodium sulfate (DSS)-induced mice colitis by regulating the balance between T helper (Th) 17 and regulatory T (Treg) cells. Methods Experimental model of UC, established by drinking water with DSS, was treated with compound sophorae decoction and mesalazine. The stool, activity, body weight of the mice, colon length and colon histopathology were observed to evaluate severity of colitis. The concentration of cytokines in colonic tissues were detected by ELISA. The expression of phosphorylated nuclear factor-kappaB (NF-κB) p65, STAT3 and phosphorylated STAT3 in colonic tissues were determined by western blotting and immunohistochemistry. The percentage of Th17 and Treg cells in spleen and mesenteric lymph nodes (MLNs) were detected by flow cytometry. The levels of transcription factor ROR-γt and FOXP3 in colon tissues were detected by qRT-PCR and immunohistochemistry. Results The aqueous extract of compound sophorae decoction was able to improve the symptoms and pathological damage of mice. The body weight of mice were increased and DAI were significantly decreased; ulcers were slighter than DSS group. The administration of compound sophorae decoction reduced the level of inflammatory factors interleukin (IL)-1β, tumor necrosis factor (TNF)-α and phospho-NF-κB p65, and also decreased the proportions of Th17 cells in spleen and MLNs and the expression of ROR-γt, IL-17A, STAT3, IL-6 in colonic tissues; while the percentage of Treg cells in spleen and MLNs and the expression of FOXP3, transforming growth factor (TGF)-β1, IL-10 in colonic tissues were upregulated. Conclusion Overall, this study suggested that compound sophorae decoction significantly improves the symptoms and the pathological damage of mice with colitis and influences the immune function by regulating Th17/Treg cell balance in DSS-induced colitis in mice. [ABSTRACT FROM AUTHOR]

[Display omitted] • Cistanche deserticola polysaccharide ameliorated the inflammation of postmenopausal osteoporosis development. • Cistanche deserticola polysaccharide regulates the proportion of Th17/Treg. • Cistanche deserticola polysaccharide restored the profiles of gut flora and short-chain fatty acids. • SCFAs modified by Cistanche deserticola polysaccharide were negatively related to postmenopausal osteoporosis. Chronic inflammation plays a critical role in the pathogenesis of postmenopausal osteoporosis (PMO). Short-chain fatty acids (SCFAs) produced by the gut microbiota (GM) have emerged as key regulators of the inflammatory response. Cistanche deserticola polysaccharide (CDP), derived from the traditional Chinese medicine Cistanche deserticola, possesses potent anti-inflammatory properties. However, the precise mechanism by which CDP modulates inflammation in PMO via the gut-bone axis remains elusive. In this study, we elucidated that CDP could effectively restore GM composition, ameliorate intestinal mucosal damage, elevate SCFA levels, rebalance the Th17/Treg cells equilibrium, attenuate the accumulation of proinflammatory cytokines, potentially facilitate osteoblast differentiation, potentially suppress osteoclastogenesis, and enhance bone microarchitecture in PMO mice. Collectively, our findings provided compelling evidence that CDP alleviated PMO-associated inflammation, potentially mediated through the intricate interplay between GM-derived SCFAs and the Th17/Treg cells. [ABSTRACT FROM AUTHOR]

Ulcerative colitis (UC) is a chronic inflammatory disease of the colon characterized by immune dysregulation. Restoration of the balance between regulatory T (Tregs) and T helper 17 (Th17) cells improves UC symptoms. Human amniotic epithelial cells (hAECs) have emerged as a promising therapeutic option for UC because of their immunomodulatory properties. In this study, we aimed to optimize and maximize the therapeutic potential of hAECs by pre-treating them with tumor necrosis factor (TNF)-α and interferon (IFN)-γ (pre-hAECs) for UC treatment. We evaluated the efficacy of hAECs and pre-hAECs in treating dextran sulfate sodium (DSS)-induced colitis mice. Compared to hAECs, pre-hAECs were found to be more effective in alleviating colitis in acute DSS mouse models than in the controls. Additionally, pre-hAEC treatment significantly reduced weight loss, shortened the colon length, decreased the disease activity index, and effectively maintained the recovery of colon epithelial cells. Furthermore, pre-hAEC treatment significantly inhibited the production of pro-inflammatory cytokines, such as interleukin (IL)-1β and TNF-α, and promoted the expression of anti-inflammatory cytokines, such as IL-10. Both in vivo and in vitro studies revealed that pre-treatment with hAECs significantly increased the number of Treg cells, decreased the numbers of Th1, Th2, and Th17 cells, and regulated the balance of Th17/Treg cells. In conclusion, our results revealed that hAECs pre-treated with TNF-α and IFN-γ were highly effective in treating UC, suggesting their potential as therapeutic candidates for UC immunotherapy., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Atractylodes macrocephala Koidz. is one of the most frequently used traditional Chinese medicines for the treatment of ulcerative colitis (UC). The beneficial effect of polysaccharide from Atractylodes macrocephala Koidz. (PAMK) on UC has been reported, while the underlying mechanism and target remain unclear. In this study, we systematically investigated the therapeutic effect and the underlying mechanism of PAMK in UC based on a mouse model of dextran sodium sulfate (DSS)-induced colitis. PAMK treatment (100 mg/kg, 200 mg/kg and 400 mg/kg) significantly ameliorated DSS-induced colitis, manifested as a reduction in weight loss, disease activity index (DAI), colon shortening, spleen index and histological score. Moreover, PAMK treatment inhibited inflammation and improved the integrity of the intestinal barrier in colitis mice. Mechanistically, microarray analysis determined the critical role of the immunoregulatory effect of PAMK in alleviating UC. Flow cytometry analysis further demonstrated that PAMK treatment regulated the balance between T helper (Th) 17 and regulatory T (Treg) cells in the mesenteric lymph nodes (MLN) and spleen in mice with colitis. In addition, PAMK treatment downregulated the expression of IL-6 and suppressed the phosphorylation of STAT3. Together, these data revealed that PAMK treatment alleviated DSS-induced colitis by regulating the Th17/Treg cell balance, which may be dependent on the inhibition of the IL-6/STAT3 signaling pathway. Our study is the first to elucidate that the underlying mechanism by which PAMK treatment alleviates DSS-induced colitis is associated with an improved the Th17/Treg cell balance. Collectively, the study provides evidence for the potential of PAMK to treat UC., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Yang, Zhang, Taha, Abdelmotalab, Wen, Yuan, Zhao, Li, Liao, Huang, Jiang, Chu, Jiao and Sun.)

Mechanism of miR-155 regulating T cell differentiation through Jarid2/Wnt/β-catenin pathway • miR-155 antagomir can relieve DSS-induced colitis. • miR-155 antagomir can regulate Th17/Treg cell balance of UC intestinal mucosa. • miR-155 antagomir may regulate UC intestinal mucosal immune function through Jarid2/Wnt/β-catenin pathway. Th subsets particularly T helper 17 and regulatory T cells play a critical role in immune balance in colonic mucosa of Inflammatory Bowel Disease. Recent studies have indicated miR-155 is overexpressed in the colonic mucosa in IBD patients. Thus, whether and how miR-155 influences Th17/Treg cell balance in IBD patients is worthy of researching. We divided mice into four groups: the mice oral administration of 3.0 % DSS in fresh drinking water for 7 days except normal group. In this period, starting from the fifth day, the miR-155 and NC antagomir group were carried out by intraperitoneal injection of miR-155 antagomirs and corresponding negative controls. In vitro, we isolated naïve CD4+T cells and divided into two groups: the cells were transfected with mmu-miR-155-5p inhibitor or corresponding negative controls and then induced differentiation. We found miR-155 antagomir can reach colon tissues in DSS-induced colitis and indeed ameliorated DSS-induced experimental colitis. Subsequently, we proved the levels of Th17 cells in spleens and Mesenteric lymph nodes and its associated IL-6, IL-17A and RORγt in colonic tissues were dramatically decreased and TGF-β1 raised in DSS + miR-155 antagomir group. However, miR-155 antagomir significantly increased the expression of Tregs. In vitro, we found miR-155 inhibitor could improve the Tregs but decrease Th17 cells. Finally, we dig out that Jarid2 was apparently improved by miR-155 antagomir, Wnt/β-catenin and its associated T cell factor-4 (TCF-4) and Cyclin D1 expression were positively correlated with Jarid2. Silencing of miR-155 attenuates DSS-induced colitis by regulating Th17/Treg cell balance and Jarid2/Wnt/β-catenin participated in the process. [ABSTRACT FROM AUTHOR]