Vitamin D reduces the differentiation and expansion of Th17 cells in young asthmatic children

Hamzaoui, A.; Berraies, A.; Hamdi, Besma; Kaabachi, Wajih; Ammar, Jamel; Hamzaoui, Kamel

doi:10.1016/j.imbio.2014.07.009

Cited by 58 publications

(40 citation statements)

References 35 publications

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“…This notion was further supported by findings that H. hepaticus infection and induction of colitis relied on host IL-23 and Th17 (Kullberg et al, 2006; Morrison et al, 2013). On the other hand, vitamin D signaling could suppress Th17 cytokine production (Chang et al, 2010), and induce CD4 + CD25 + Foxp3 + regulatory T cells (Takeda et al, 2010; Hamzaoui et al, 2014). Enterohepatic Helicobacter species including H. hepaticus are prevalent in mice from commercial and academic institutions worldwide (Shames et al, 1995; Taylor et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models

et al. 2016

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Metabolic syndrome (MetS), characterized as obesity, insulin resistance, and non-alcoholic fatty liver diseases (NAFLD), is associated with vitamin D insufficiency/deficiency in epidemiological studies, while the underlying mechanism is poorly addressed. On the other hand, disorder of gut microbiota, namely dysbiosis, is known to cause MetS and NAFLD. It is also known that systemic inflammation blocks insulin signaling pathways, leading to insulin resistance and glucose intolerance, which are the driving force for hepatic steatosis. Vitamin D receptor (VDR) is highly expressed in the ileum of the small intestine, which prompted us to test a hypothesis that vitamin D signaling may determine the enterotype of gut microbiota through regulating the intestinal interface. Here, we demonstrate that high-fat-diet feeding (HFD) is necessary but not sufficient, while additional vitamin D deficiency (VDD) as a second hit is needed, to induce robust insulin resistance and fatty liver. Under the two hits (HFD+VDD), the Paneth cell-specific alpha-defensins including α-defensin 5 (DEFA5), MMP7 which activates the pro-defensins, as well as tight junction genes, and MUC2 are all suppressed in the ileum, resulting in mucosal collapse, increased gut permeability, dysbiosis, endotoxemia, systemic inflammation which underlie insulin resistance and hepatic steatosis. Moreover, under the vitamin D deficient high fat feeding (HFD+VDD), Helicobacter hepaticus, a known murine hepatic-pathogen, is substantially amplified in the ileum, while Akkermansia muciniphila, a beneficial symbiotic, is diminished. Likewise, the VD receptor (VDR) knockout mice exhibit similar phenotypes, showing down regulation of alpha-defensins and MMP7 in the ileum, increased Helicobacter hepaticus and suppressed Akkermansia muciniphila. Remarkably, oral administration of DEFA5 restored eubiosys, showing suppression of Helicobacter hepaticus and increase of Akkermansia muciniphila in association with resolving metabolic disorders and fatty liver in the HFD+VDD mice. An in vitro analysis showed that DEFA5 peptide could directly suppress Helicobacter hepaticus. Thus, the results of this study reveal critical roles of a vitamin D/VDR axis in optimal expression of defensins and tight junction genes in support of intestinal integrity and eubiosis to suppress NAFLD and metabolic disorders.

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Section: Discussionmentioning

confidence: 99%

Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models

et al. 2016

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“…Previous reports have shown that T cells, B cells, dendritic cells (DCs), monocytes, and macrophages are all influenced by the regulation of 1,25(OH) 2 D 3 [7811121314151617181920212223]. 1,25(OH) 2 D 3 inhibits T-cell proliferation [11, 12]; facilitates induction of Foxp3 + T regulatory (Treg) cells [13]; suppresses the differentiation, maintenance, bioactivity, and transcription of Th17 cells [1415]; and induces the switch from Th1 to Th2 by decreasing the Th1 response via regulation of antigen presenting cells and enhancing Th2 cell development [1617].…”

Section: Vitamin D and The Immune Systemmentioning

confidence: 99%

The role of vitamin D in allergic rhinitis

Tian

Cheng

2017

Asia Pacific Allergy

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Recent studies suggest that vitamin D is related to allergic rhinitis (AR). In this review, we first discuss the physiology and metabolism of vitamin D, then we review the function of vitamin D in the immune system, and above all, we highlight the current research regarding the role of vitamin D in AR. Finally, we find that there are both experimental and clinical studies showing that vitamin D is associated with AR, although the results are not consistent and even conflicting. Evidences from those clinical studies show a slightly tendency that serum vitamin D level might be inversely associated with the risk of AR. Meanwhile, it seems that gender and age may influence the relationship between vitamin D and AR. However, because of the heterogeneity in defining AR, differences in study design and so on, all these findings need to be confirmed by further studies. Additional clinical studies as well as experimental research are needed to better understand how vitamin D influences AR.

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“…The generally recognized MS risk factor hypovitaminosis D (Ascherio & Munger, 2007;Hanwell & Banwell, 2011) is defined as a 25-hydroxyvitamin D (25(OH)D) concentration below 50 nmol/L and is prevalent in approximately 57% of German adults (Hintzpeter, Mensink, Thierfelder, Müller, & Scheidt-Nave, 2008). Experimental data show that vitamin D (VD) possesses anti-inflammatory and immunomodulatory properties through inhibition of dendritic cell differentiation, induction of T regulatory cells, blockage of Th17 differentiation, and down-regulation of Th1 immune responses (Farias et al, 2013;Hamzaoui et al, 2014;Lemire, Archer, Beck, & Spiegelberg, 1995). Concordantly, several studies have found an inverse correlation between serum 25(OH)D concentration and disease activity in MS patients (Brola et al, 2016;Pierrot-Deseilligny, Rivaud-Péchoux, Clerson, de Paz, & Souberbielle, 2012;Rotstein et al, 2015;Simpson et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D supplementation differentially affects seasonal multiple sclerosis disease activity

Miclea

Miclea²,

Pistor

et al. 2017

Brain and Behavior

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Vitamin D reduces the differentiation and expansion of Th17 cells in young asthmatic children

Cited by 58 publications

References 35 publications

Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models

Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models

The role of vitamin D in allergic rhinitis

Vitamin D supplementation differentially affects seasonal multiple sclerosis disease activity

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