Limited effects of dietary curcumin on Th-1 driven colitis in IL-10 deficient mice suggest an IL-10-dependent mechanism of protection

Larmonier, Claire B.; Uno, Jennifer K.; Lee, Kang Moon; Karrasch, Thomas; Laubitz, Daniel; Thurston, Robert D.; Midura-Kiela, Monica T.; Ghishan, Fayez K.; Sartor, R. Balfour; Jobin, Christian; Kiela, Pawel R.

doi:10.1152/ajpgi.90365.2008

Cited by 68 publications

(56 citation statements)

References 52 publications

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“…However, in agreement with our data, curcumin had been shown to enhance IL-10 production by human T cells and mouse macrophages [48,49]. Furthermore, curcumin inhibition of NF-kB was dependent on IL-10, in that curcumin failed to inhibit NF-kB activity in IL-10 À/À mice [50]. Our data demonstrated that curcumin did not modulate IL-10-deficient DC to induce Treg, which could be one explanation on limited effects of curcumin on Th1-driven colitis in IL-10 À/À mice [50].…”

Section: Discussionsupporting

confidence: 91%

“…Furthermore, curcumin inhibition of NF-kB was dependent on IL-10, in that curcumin failed to inhibit NF-kB activity in IL-10 À/À mice [50]. Our data demonstrated that curcumin did not modulate IL-10-deficient DC to induce Treg, which could be one explanation on limited effects of curcumin on Th1-driven colitis in IL-10 À/À mice [50]. Addition of anti-IL-10R or anti-TGF-b Ab also blocked induction of Treg.…”

Section: Discussionmentioning

confidence: 99%

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Curcumin induces the tolerogenic dendritic cell that promotes differentiation of intestine‐protective regulatory T cells

Cong¹,

Wang²,

Konrad³

et al. 2009

Eur J Immunol

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The gut is home to a large number of Treg, with both CD4 1 CD25 1 Treg and bacterial antigen-specific Tr1 cells present in normal mouse intestinal lamina propria. It has been shown recently that intestinal mucosal DC are able to induce Foxp3 1 Treg through production of TGF-b plus retinoic acid (RA). However, the factors instructing DC toward this mucosal phenotype are currently unknown. Curcumin has been shown to possess a number of biologic activities including the inhibition of NF-jB signaling. We asked whether curcumin could modulate DC to be tolerogenic whose function could mimic mucosal DC. We report here that curcumin modulated BM-derived DC to express ALDH1a and IL-10. These curcumin-treated DC induced differentiation of naïve CD4 1 T cells into Treg resembling Treg in the intestine, including both CD4 1 CD25 1 Foxp3 1 Treg and IL-10-producing Tr1 cells. Such Treg induction required IL-10, TGF-b and retinoic acid produced by curcumin-modulated DC. Cell contact as well as IL-10 and TGF-b production were involved in the function of such induced Treg. More importantly, these Treg inhibited antigen-specific T-cell activation in vitro and inhibited colitis due to antigen-specific pathogenic T cells in vivo.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Curcumin induces the tolerogenic dendritic cell that promotes differentiation of intestine‐protective regulatory T cells

Cong¹,

Wang²,

Konrad³

et al. 2009

Eur J Immunol

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“…Numerous reports have been published suggesting that oral administration of curcumin down-regulates TNF-a expression both in the serum and in the tissue of animals (Nanji et al, 2003;Yao et al, 2004;Sharma et al, 2007a;Billerey-Larmonier et al, 2008;Larmonier et al, 2008;Ung et al, 2010;El-Moselhy et al, 2011;Gutierres et al, 2012) ( Table 2). Attenuation of TNF-a levels by curcumin has been noted in mice (Leyon and Kuttan, 2003), rats (Siddiqui et al, 2006) and rabbits (Yao et al, 2004;Huang et al, 2008).…”

Section: Suppression Of Tnf By Curcumin In Vivomentioning

confidence: 99%

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

320

235

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TNFs are major mediators of inflammation and inflammation-related diseases, hence, the United States Food and Drug Administration (FDA) has approved the use of blockers of the cytokine, TNF-a, for the treatment of osteoarthritis, inflammatory bowel disease, psoriasis and ankylosis. These drugs include the chimeric TNF antibody (infliximab), humanized TNF-a antibody (Humira) and soluble TNF receptor-II (Enbrel) and are associated with a total cumulative market value of more than $20 billion a year. As well as being expensive ($15 000-20 000 per person per year), these drugs have to be injected and have enough adverse effects to be given a black label warning by the FDA. In the current report, we describe an alternative, curcumin (diferuloylmethane), a component of turmeric (Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-a action and production in in vitro models, in animal models and in humans. In addition, we provide evidence for curcumin's activities against all of the diseases for which TNF blockers are currently being used. Mechanisms by which curcumin inhibits the production and the cell signalling pathways activated by this cytokine are also discussed. With health-care costs and safety being major issues today, this golden spice may help provide the solution. LINKED ARTICLESThis article is part of a themed section on Emerging Therapeutic Aspects in Oncology. To view the other articles in this section visit http://dx

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“…This observation is in line with a previous study showing minimal effect of curcumin on inflammation in Il10 −/− mice. 47 Although histological score indicated significant improvement in the distal colon of Il10 −/− /AOM mice fed 0.5% curcumin, this is most likely the result of diminished hyperplasia, submucosal edema, smooth muscle thickness, and dysplastic and neoplastic changes, which were all integral parts of the scoring system. Mucosal cytokine expression, a more objective measure of mucosal inflammatory tone, with the exception of IFNγ in the distal colon, did not indicate a significant reduction of inflammatory response in AOM/Il10 −/− mice fed control of curcumin-supplemented diet (Fig.…”

Section: Discussionmentioning

confidence: 95%

“…22,23 Higher dose (1%) proved detrimental in the Il10 −/− mouse model, an observation that was anticipated based on our previous studies with Il10 −/− model. 47 The chemopreventive effects of curcumin did not correspond with a strong suppression of mucosal inflammatory responses. This observation is in line with a previous study showing minimal effect of curcumin on inflammation in Il10 −/− mice.…”

Section: Discussionmentioning

confidence: 96%

275 The Role of Curcumin in Modulating Colonic Microbiota During Colitis and Colon Cancer Prevention

McFadden¹,

Larmonier²,

Midura-Kiela³

et al. 2014

Gastroenterology

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Background-Intestinal microbiota influences the progression of colitis-associated colorectal cancer (CAC). With diet being a key determinant of the gut microbial ecology, dietary interventions are an attractive avenue for the prevention of CAC. Curcumin is the most active constituent of the ground rhizome of the Curcuma Longa plant, which has been demonstrated to have anti-inflammatory, anti-oxidative and anti-proliferative properties.

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Limited effects of dietary curcumin on Th-1 driven colitis in IL-10 deficient mice suggest an IL-10-dependent mechanism of protection

Abstract: Larmonier CB, Uno JK, Lee KM, Karrasch T, Laubitz D, Thurston R, Midura-Kiela MT, Ghishan FK, Sartor RB, Jobin C, Kiela PR. Limited effects of dietary curcumin on Th-1 driven colitis in IL-10 deficient mice suggest an IL-10-dependent mechanism of protection.

Cited by 68 publications

References 52 publications

Curcumin induces the tolerogenic dendritic cell that promotes differentiation of intestine‐protective regulatory T cells

Curcumin induces the tolerogenic dendritic cell that promotes differentiation of intestine‐protective regulatory T cells

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

275 The Role of Curcumin in Modulating Colonic Microbiota During Colitis and Colon Cancer Prevention

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