High fat diet exacerbates dextran sulfate sodium induced colitis through disturbing mucosal dendritic cell homeostasis

Cheng, Lü; Jin, Han Seung; Qiang, Yetao; Wu, Shuiyun; Cheng, Yan; Han, Mutian; Xiao, Tengfei; Yan, Nannan; An, Huazhang; Zhou, Xiaoming; Shao, Qixiang; Sheng, Xia

doi:10.1016/j.intimp.2016.08.018

Cited by 80 publications

(64 citation statements)

References 62 publications

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“…Indeed, rIL-33 administration resulted in an increased ALDH1A1 and TSLP expression in intestine epithelium cells, resulting in an increased conversion of CD103+ DCs (24). Moreover, in accordance with other reports (25, 26), we also observed loss of CD103+ DCs during colonic inflammation in DSS-induced colitis (data not shown). Notably, epithelium cell from IBDs patients, which were damaged during the abnormal immune response, showed an impaired function in CD103+ DCs propagation (20).…”

Section: Discussionsupporting

confidence: 93%

“…Our previous study also demonstrated that the protective effect of IL-33 is predominantly dependent on Treg cell expansion, which was closely associated with upregulation of CD103+IDO+ DCs (24). Epithelium cell-derived TGF-β and retinoic acid (RA) were found to be required for CD103+ DC tolerogenic phenotype conversion, and epithelium cell from IBDs patients showed an impaired function in CD103+ DC conversion (20), which result in a diminishment of CD103+ DCs in IBDs (25, 26). Although abnormalities in both Th1 and Th2 immune responses were detected in ulcerative colitis (UC) patients, the Th2 immune response is considered to play a predominant role (15).…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-4 Inhibits Regulatory T Cell Differentiation through Regulating CD103+ Dendritic Cells

Chen

Zhang

et al. 2017

Front. Immunol.

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CD103+ dendritic cells (DCs) have been shown to play a crucial role in the pathogenesis of inflammatory bowel diseases (IBDs) through educating regulatory T (Treg) cells differentiation. However, the mechanism of CD103+ DCs subsets differentiation remains elusive. Interleukin (IL)-4 is a pleiotropic cytokine that is upregulated in certain types of inflammation, including IBDs and especially ulcerative colitis. However, the precise role of IL-4 in the differentiation of CD103+ DCs subpopulation remains unknown. In this study, we observed a repressive role of IL-4 on the CD103+ DCs differentiation in both mouse and human. High-dose IL-4 inhibited the CD103+ DC differentiation. In comparison to CD103− DCs, CD103+ DCs expressed high levels of the co-stimulatory molecules and indoleamine 2,3-dioxygenase (IDO). Interestingly, IL-4 diminished IDO expression on DCs in a dose-dependent manner. Besides, high-dose IL-4-induced bone marrow-derived DCs, and monocyte-derived DCs revealed mature DCs profiles, characterized by increased co-stimulatory molecules and decreased pinocytotic function. Furthermore, DCs generated under low concentrations of IL-4 favored Treg cells differentiation, which depend on IDO produced by CD103+ DCs. Consistently, IL-4 also reduced the frequency of CD103+ DC in vivo. Thus, we here demonstrated that the cytokine IL-4 involved in certain types of inflammatory diseases by orchestrating the functional phenotype of CD103+ DCs subsets.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Interleukin-4 Inhibits Regulatory T Cell Differentiation through Regulating CD103+ Dendritic Cells

Chen

Zhang

et al. 2017

Front. Immunol.

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“…For studies showing null ypsin; AA-Arachidonic Acid; AECs-Airway spase-1; CCR7-C-C Chemokine Receptor Type [105] ion and ↑ recruitment to lipid rafts on the plasma membrane [83] of dietary fatty acids on innate and adaptive immune cells in vitro. For studies showing null lation or increase; A1AD-Alpha-1-Antitrypsin; AA-Arachidonic Acid; AECs-Airway TP-Adenosine Triphosphate; CASP-1-Caspase-1; CCR7-C-C Chemokine Receptor Type -Phospholipase 2; CXCL3-Chemokine (C-X-C motif) n-3 PUFA-rich diet B cells ↑ CD69 and CD40 expression [103,128] ↑ IL-6, IFN-γ, TNF-α and IL-10, IL-5, IL-13, and IL-9 expression [103,128,129] ↑ Percentage of splenic transitional, marginal zone B cells and peritoneal B1 cells [130,131] ↑ Surface expression of IgM in spleen and serum [130,131] ↑ Caecal IgA [128] Changed lipid composition of B cells and ↑ size, order and the distribution of rafts [128,129,132] SFA-rich diet Dendritic cells ↓ Tolerogenic (CD11c + CD103 + CD11b + ) and ↑ pro-inflammatory (CD11c + CD103 − CD11b + ) subpopulations in the gut [133] ↑ TLR4-dependent NLRP3 inflammasome activation and IL-1β secretion [134] Neutrophils ↓ Survival rate and ↑ bacterial proliferation in septic mice [135] ↓ Cell frequency, ↓ phagocytosis and ↓ ROS production in septic mice [135] T cells ↑ CXCR3 and ↓ CCR7 and L-selectin expression [99] ↑ Severity of the disease, ↑ Th1, and Th17 cell differentiation and ↑ T cell infiltration into the central nervous system [101,136] Positive association with several markers of inflammation, such as C-reactive protein, IL-1RA, IFN-γ and CCL5 [137] [83] une cells in vitro.…”

Section: Cell Typementioning

confidence: 99%

“…The in vivo actions of dietary FAs on DCs have been investigated in the mouse model of IBD, where animals were fed either high (HFD)-or low-fat diet [133]. HFD decreases tolerogenic (CD11c + CD103 + CD11b + ) and increases pro-inflammatory (CD11c + CD103 − CD11b + ) DCs subpopulations in the gut [133] pointing it as an important factor in IBD pathogenesis [133]. SFA intake is also related to inflammasome-mediated inflammation [134].…”

Section: Dendritic Cellsmentioning

confidence: 99%

The Influence of Dietary Fatty Acids on Immune Responses

et al. 2019

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Diet-derived fatty acids (FAs) are essential sources of energy and fundamental structural components of cells. They also play important roles in the modulation of immune responses in health and disease. Saturated and unsaturated FAs influence the effector and regulatory functions of innate and adaptive immune cells by changing membrane composition and fluidity and by acting through specific receptors. Impaired balance of saturated/unsaturated FAs, as well as n-6/n-3 polyunsaturated FAs has significant consequences on immune system homeostasis, contributing to the development of many allergic, autoimmune, and metabolic diseases. In this paper, we discuss up-to-date knowledge and the clinical relevance of the influence of dietary FAs on the biology, homeostasis, and functions of epithelial cells, macrophages, dendritic cells, neutrophils, innate lymphoid cells, T cells and B cells. Additionally, we review the effects of dietary FAs on the pathogenesis of many diseases, including asthma, allergic rhinitis, food allergy, atopic dermatitis, rheumatoid arthritis, multiple sclerosis as well as type 1 and 2 diabetes.

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“…The host microbiota can be easily modified by food. Consumption of high-fat diet (HFD) is regarded as one of the risk factors of IBD and several studies demonstrated that HFD exacerbates DSS induced colitis in animals (20, 21). We were wondering whether the effect of probiotics can be modified by HFD.…”

Section: Resultsmentioning

confidence: 99%

The probiotic effectiveness in experimental colitis is correlated with gut microbiome and host genetic features

Suwal

W³

et al. 2018

Preprint

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19Current evidence to support extensive use of probiotics in inflammatory bowel disease is 20 limited and factors contribute to the inconsistent effectiveness of clinical probiotic therapy are 21 not completely known. Here, as a proof-of-concept, we utilized Bifidobacterium longum JDM 22 301, a widely used commercial probiotic strain in China, to study potential factors that may 23 influence the beneficial effect of probiotics in experimental colitis. We found that the probiotic 24 therapeutic effect was varied across individual mouse even with the same genetic background 25 and consuming the same type of food. The different probiotic efficacy was highly correlated 26 with different microbiome features in each mouse. Consumption of a diet rich in fat can change 27 the host sensitivity to mucosal injury-induced colitis but did not change the host responsiveness 28 to probiotic therapy. Finally, the host genetic factor TLR2 was required for a therapeutic effect 29 of B. longum JDM 301. Together, our results suggest that personalized microbiome and genetic 30 features may modify the probiotic therapeutic effect.31

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High fat diet exacerbates dextran sulfate sodium induced colitis through disturbing mucosal dendritic cell homeostasis

Cited by 80 publications

References 62 publications

Interleukin-4 Inhibits Regulatory T Cell Differentiation through Regulating CD103+ Dendritic Cells

Interleukin-4 Inhibits Regulatory T Cell Differentiation through Regulating CD103+ Dendritic Cells

The Influence of Dietary Fatty Acids on Immune Responses

The probiotic effectiveness in experimental colitis is correlated with gut microbiome and host genetic features

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