Apple polyphenols require T cells to ameliorate dextran sulfate sodium-induced colitis and dampen proinflammatory cytokine expression

Abstract Ghrelin (Grln) is a peptide hormone that is predominantly produced in the stomach and stimulates appetite and induces growth hormone (GH) release. We have previously reported that ghrelin is also expressed in T cells and exerts prothymic and anti-inflammatory effects. However, the biologic relevance of T cell–derived ghrelin remains to be determined. Here, we report that acylated-bioactive ghrelin is expressed in human T cells and preferentially segregates within the lipid raft domains upon TCR ligation. The RNA interference (RNAi)–mediated down-regulation of ghrelin in primary human T cells activates IkB, and increases Th1 cytokines and IL-17 secretion. Ghrelin expression declines with increasing age in spleen and T cells and exogenous ghrelin administration in old mice reduces proinflammatory cytokines. These findings demonstrate that ghrelin functions in an autocrine and paracrine capacity to regulate proinflammatory cytokine expression in human and murine T cells and may contribute in regulating “inflamm-aging.”

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Rotavirus acceleration of murine type 1 diabetes is associated with increased MHC class I-restricted antigen presentation by B cells and elevated proinflammatory cytokine expression by T cells

Virus Research ◽

10.1016/j.virusres.2013.11.009 ◽

2014 ◽

Vol 179 ◽

pp. 73-84 ◽

Cited By ~ 10

Author(s):

Jessica A. Pane ◽

Nicole L. Webster ◽

Christel Zufferey ◽

Barbara S. Coulson

Keyword(s):

T Cells ◽

Type 1 Diabetes ◽

B Cells ◽

Antigen Presentation ◽

Mhc Class I ◽

Proinflammatory Cytokine ◽

Cytokine Expression ◽

Class I ◽

Proinflammatory Cytokine Expression

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Inhibition of Proinflammatory Cytokines in Cutibacterium acnes-Induced Inflammation in HaCaT Cells by Using Buddleja davidii Aqueous Extract

International Journal of Inflammation ◽

10.1155/2020/8063289 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Anh Thu Nguyen ◽

Ki-young Kim

Keyword(s):

Proinflammatory Cytokines ◽

Proinflammatory Cytokine ◽

Treatment Options ◽

Mapk Signaling ◽

Cytokine Expression ◽

Proinflammatory Cytokine Expression ◽

Cutibacterium Acnes ◽

Anti Inflammatory ◽

New Treatment ◽

Hacat Keratinocyte

Acne is an inflammatory skin disorder; although some anti-inflammatory medicines for treating acne are available in a market, they have considerable side effects; therefore, new treatment options are needed. In the present study, among the 16 aqueous extracts of plants collected from Jeju Island in Korea which are used to test anti-inflammatory activity, B. davidii showed the strong decline of the proinflammatory cytokine expression against the inflammatory process caused by C. acnes in Human HaCaT keratinocyte cells. B. davidii downregulated the expression of 57% of COX-2, 41% of iNOS, and proinflammatory cytokines 29% of TNF-α, 32% of IL-1β, 21% of IL-6, and 35% of IL-8. Furthermore, B. davidii inhibited NF-κB and MAPK signaling cascades in keratinocytes that activated by toll-like receptor 2 (TLR-2) in response to C. acnes. Given those results, B. davidii is a potential agent to reduce the proinflammatory cytokine expression against C. acnes-induced inflammation and might provide an alternative to the current medications.

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Involvement of CD4+ T Cells in the Development of Dextran Sulfate Sodium-Induced Experimental Colitis and Suppressive Effect of IgG on Their Action

General Pharmacology The Vascular System ◽

10.1016/s0306-3623(98)00004-4 ◽

1998 ◽

Vol 31 (3) ◽

pp. 477-481 ◽

Cited By ~ 44

Author(s):

Nahoko Shintani ◽

Tsunetaka Nakajima ◽

Tadao Okamoto ◽

Takao Kondo ◽

Norifumi Nakamura ◽

...

Keyword(s):

T Cells ◽

Cd4 T Cells ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Experimental Colitis ◽

Suppressive Effect

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Acetylcholine-producing T cells augment innate immune-driven colitis but are redundant in T cell-driven colitis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00067.2019 ◽

2019 ◽

Vol 317 (5) ◽

pp. G557-G568 ◽

Cited By ~ 2

Author(s):

Rose A. Willemze ◽

David J. Brinkman ◽

Olaf Welting ◽

Patricia H. P. van Hamersveld ◽

Caroline Verseijden ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Nerve Stimulation ◽

Vagus Nerve Stimulation ◽

Inflammatory Cytokine ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Innate Immune ◽

Cytokine Levels ◽

Colitis Model

Clinical trials suggest that vagus nerve stimulation presents an alternative approach to classical immune suppression in Crohn's disease. T cells capable of producing acetylcholine (ChAT+ T cells) in the spleen are essential mediators of the anti-inflammatory effect of vagus nerve stimulation. Besides the spleen, ChAT+ T cells are found abundantly in Peyer’s patches of the small intestine. However, the role of ChAT+ T cells in colitis pathogenesis is unknown. Here, we made use of CD4creChATfl/fl mice (CD4ChAT−/− mice) lacking ChAT expression specifically in CD4+ T cells. Littermates (ChATfl/fl mice) served as controls. In acute dextran sulfate sodium (DSS)-induced colitis (7 days of 2% DSS in drinking water), CD4ChAT−/− mice showed attenuated colitis and lower intestinal inflammatory cytokine levels compared with ChATfl/fl mice. In contrast, in a resolution model of DSS-induced colitis (5 days of 2% DSS followed by 7 days without DSS), CD4ChAT−/− mice demonstrated a worsened colitis recovery and augmented colonic histological inflammation scores and inflammatory cytokine levels as compared with ChATfl/fl mice. In a transfer colitis model using CD4+CD45RBhigh T cells, T cells from CD4ChAT−/− mice induced a similar level of colitis compared with ChATfl/fl T cells. Together, our results indicate that ChAT+ T cells aggravate the acute innate immune response upon mucosal barrier disruption in an acute DSS-induced colitis model, whereas they are supporting the later resolution process of this innate immune-driven colitis. Surprisingly, ChAT expression in T cells seems redundant in the context of T cell-driven colitis. NEW & NOTEWORTHY By using different mouse models of experimental colitis, we provide evidence that in dextran sulfate sodium-induced colitis, ChAT+ T cells capable of producing acetylcholine worsen the acute immune response, whereas they support the later healing phase of this innate immune-driven colitis.

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The Effect of Exercise and Nutritional Supplementation on Proinflammatory Cytokine Expression in Young Racehorses During Training

Journal of Equine Veterinary Science ◽

10.1016/j.jevs.2012.03.017 ◽

2012 ◽

Vol 32 (12) ◽

pp. 805-815 ◽

Cited By ~ 22

Author(s):

David W. Horohov ◽

Stephen T. Sinatra ◽

Raj K. Chopra ◽

Stanley Jankowitz ◽

Alejandra Betancourt ◽

...

Keyword(s):

Proinflammatory Cytokine ◽

Cytokine Expression ◽

Nutritional Supplementation ◽

Proinflammatory Cytokine Expression

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6,7,4′-Trihydroxyflavanone Protects against Dextran Sulfate Sodium-Induced Colitis by Regulating the Activity of T Cells and Colon Cells In Vivo

International Journal of Molecular Sciences ◽

10.3390/ijms22042083 ◽

2021 ◽

Vol 22 (4) ◽

pp. 2083

Author(s):

Hyun-Su Lee ◽

Gil-Saeng Jeong

Keyword(s):

T Cells ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Cell Activity ◽

Bioactive Molecules ◽

Colon Cells ◽

Colon Cell ◽

Ht 29 ◽

Colitis Model

Colitis is a multifactorial disorder that mostly occurs in the gastrointestinal tract. Despite improvements in mucosal inflammation research, little is known regarding the small bioactive molecules that are beneficial for regulating T cells and colon cell activity. 6,7,4′-trihydroxyflavanone (THF) is a flavanone that possesses anti-osteoclastogenesis activity and exerts protective effects against methamphetamine-induced immunotoxicity. Whether THF mitigates intestinal inflammation by regulating T cells and colon cell activity remains unknown. In the present study, Jurkat and HT-29 cells were used for in vitro experiments, and dextran sulfate sodium (DSS)-induced colitis model in mice was used for in vivo experiment. We observed that THF did not have a negative effect on the viability of Jurkat and HT-29 cells. Quantitative PCR and Western blot analysis revealed that THF regulates the activity of Jurkat cells and HT-29 cells via the NFκB and MAPK pathways under stimulated conditions. In the DSS-induced colitis model, oral administration of THF attenuated the manifestations of DSS-induced colitis, including a reduction in body weight, shrinkage of the colon, and enhanced expression of pro-inflammatory cytokines in the colon and mesenteric lymph nodes. These data suggest that THF alleviates DSS-induced colitis by modulating the activity of T cells and colon cells in vivo.

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