Analysis of murine and human Treg subsets in inflammatory bowel disease

Sun, Xiaoyun; He, Shaoheng; Lv, Changlong; Sun, Xun; Wang, Junling; Zheng, Wenjiao; Wang, Danan

doi:10.3892/mmr.2017.6912

Cited by 32 publications

(26 citation statements)

References 20 publications

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“…Indeed, there is evidence that IL-10 exhibits a suppressive and modulatory action by downregulating the activation of the immune cells and co-stimulatory molecules, thus protecting from immune-related mucosal injury during the chronic stage in IBD. Deficiency in IL-10 receptor [42], as well as changes in the subset and in the number of Treg in colonic mucosa and blood, induce the development of severe IBD in mice and humans [41,43]. As obtained using longer administration periods [25], in the current experiment, the treatment with BC for 7 days reduced the increase of IL-10 gene expression in TNBS-induced colitis in mice.…”

Section: Discussionsupporting

confidence: 58%

“…Treg and the products of their secretion, the anti-inflammatory cytokines IL-10 and Transforming Growth Factor-β (TGF-β) may play an essential role in the gastrointestinal homeostasis [10,41]. Indeed, there is evidence that IL-10 exhibits a suppressive and modulatory action by downregulating the activation of the immune cells and co-stimulatory molecules, thus protecting from immune-related mucosal injury during the chronic stage in IBD.…”

Section: Discussionmentioning

confidence: 99%

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The Prophylactic Use of Bovine Colostrum in a Murine Model of TNBS-Induced Colitis

Menchetti

Curone

Filipescu³

et al. 2020

Animals

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Simple Summary: Colostrum is the first milk secreted by the mammary glands, and it is very rich in bioactive components. Recently, the importance of bovine colostrum (BC) as a nutraceutical product has been emerging with regards to gastrointestinal diseases. One of the most widespread gastrointestinal disorders is the inflammatory bowel disease (IBD), a multifactorial chronic condition that has a powerful impact on the social life of millions of people. Because current therapy protocols neither ensure complete recovery from IBD nor are free of secondary side effects, the present study assessed the impact of a short-term prophylactic oral administration of BC in a murine model of TNBS-induced colitis. BC administration was both well tolerated and did not induce any pathological symptoms. It considerably modulated the response to inflammation through modifications of the TLR4 and cytokines gene expression profiles as well as that of the intestinal microbiota. Although further studies are needed to develop a precise therapeutic protocol of BC administration, it seems to have the potential to be used as a natural supplement in the treatment of IBD.Abstract: This study investigated the effects of a short-term administration of bovine colostrum (BC) in a TNBS model of induced colitis. Colitis was induced by TNBS treatment after seven days of BC (BC group, n = 12) or saline (control group, n = 12) administration in mice. Clinical signs, histopathological characteristics, expression levels of Toll-like receptor 4 (TLR4), pro-and anti-inflammatory cytokines, and microbial composition were assessed. BC was well tolerated and did not induce any histological damage or clinical symptoms. After TNBS treatment, the BC group showed a reduction in body weight (BW) loss compared to Control (p < 0.05). Moreover, expression levels of TLR4 (p < 0.01), Interleukin-1β (IL-1β; p < 0.001), Interleukin-8 (IL-8; p < 0.001), and Interleukin-10 (IL-10; p < 0.001) were lower in mice administered with BC. Finally, Escherichia coli were higher (p < 0.05), while Enterococci (p < 0.001), Lactobacillus spp. (p < 0.001), and Bifidobacterium spp. (p < 0.05) were lower in Control than BC group. This study confirms that pre-treatment with BC modulates the expression of genes and the count of microbes involved in the etiopathogenesis of colitis.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

The Prophylactic Use of Bovine Colostrum in a Murine Model of TNBS-Induced Colitis

Menchetti

Curone

Filipescu³

et al. 2020

Animals

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“…The unbalanced cellular immune responses seem to be mainly responsible for the initiation and development of the inflammation in IBD. These adaptive cellular responses involve activation of T helper (Th) lymphocytes and suppression of the activity of T regulatory (Treg) cells . We examined the subtypes of T lymphocytes to investigate whether IL‐35 recombinant protein also acted on T cells to play its regulative role.…”

Section: Resultsmentioning

confidence: 99%

IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells

Wang

Mao

Zhang

et al. 2017

J Cellular Molecular Medi

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Interleukin-35 (IL-35), a member of the IL-12 family, functions as a new anti-inflammatory factor involved in arthritis, psoriasis, inflammatory bowel disease (IBD) and other immune diseases. Although IL-35 can significantly prevent the development of inflammation in many diseases, there have been no early studies accounting for the role of IL-35 recombinant protein in IBD and psoriasis. In this study, we assessed the therapeutic potential of IL-35 recombinant protein in three well-known mouse models: the dextransulfate sodium ( Further analysis demonstrated that IL-35 recombinant protein may regulate inflammation through promoting the secretion of IL-10 and inhibiting the expression of pro-inflammatory cytokines such as IL-6, TNF-a and IL-17 in acute colitis model. In addition, lower dose of IL-35 recombinant protein could achieve long-term treatment effects as TNF-a monoclonal antibody did in the psoriasis mouse. In summary, the remarkable therapeutic effects of IL-35 recombinant protein in acute colitis and psoriasis mouse models indicated that IL-35 recombinant protein had a variety of anti-inflammatory effects and was expected to become an effective candidate drug for the treatment of inflammatory diseases.

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“…However, in the acute IBD model that was used in the present study, no significant changes were found in the expression levels of K Ca 3.1 or HDAC3 in splenic CD4 + CD25 + cells ( Figure S6 ). T reg cells decreased during the active stage of IBD and increased during the remission period at the chronic stage of IBD [ 41 ]. Further studies are needed to elucidate the pathophysiological significance of HDAC3-mediated K Ca 3.1 regulation in the development and function of T reg cells using chronic IBD models.…”

Section: Discussionmentioning

confidence: 99%

Histone Deacetylases Enhance Ca2+-Activated K+ Channel KCa3.1 Expression in Murine Inflammatory CD4+ T Cells

Matsui

Terasawa

Kajikuri

et al. 2018

IJMS

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The up-regulated expression of the Ca2+-activated K+ channel KCa3.1 in inflammatory CD4+ T cells has been implicated in the pathogenesis of inflammatory bowel disease (IBD) through the enhanced production of inflammatory cytokines, such as interferon-γ (IFN-γ). However, the underlying mechanisms have not yet been elucidated. The objective of the present study is to clarify the involvement of histone deacetylases (HDACs) in the up-regulation of KCa3.1 in the CD4+ T cells of IBD model mice. The expression levels of KCa3.1 and its regulators, such as function-modifying molecules and transcription factors, were quantitated using a real-time polymerase chain reaction (PCR) assay, Western blotting, and depolarization responses, which were induced by the selective KCa3.1 blocker TRAM-34 (1 μM) and were measured using a voltage-sensitive fluorescent dye imaging system. The treatment with 1 μM vorinostat, a pan-HDAC inhibitor, for 24 h repressed the transcriptional expression of KCa3.1 in the splenic CD4+ T cells of IBD model mice. Accordingly, TRAM-34-induced depolarization responses were significantly reduced. HDAC2 and HDAC3 were significantly up-regulated in the CD4+ T cells of IBD model mice. The down-regulated expression of KCa3.1 was observed following treatments with the selective inhibitors of HDAC2 and HDAC3. The KCa3.1 K+ channel regulates inflammatory cytokine production in CD4+ T cells, mediating epigenetic modifications by HDAC2 and HDAC3.

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Analysis of murine and human Treg subsets in inflammatory bowel disease

Cited by 32 publications

References 20 publications

The Prophylactic Use of Bovine Colostrum in a Murine Model of TNBS-Induced Colitis

The Prophylactic Use of Bovine Colostrum in a Murine Model of TNBS-Induced Colitis

IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells

Histone Deacetylases Enhance Ca2+-Activated K+ Channel KCa3.1 Expression in Murine Inflammatory CD4+ T Cells

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