Abstract
Immune cells not only affect tissue homeostasis at the site of inflammation but also exert systemic effects contributing to multiple chronic conditions. Recent evidence clearly supports an altered T helper 17/regulatory T cell (Th17/Treg) balance leading to the development and progression of inflammatory diseases that not only affect the gastrointestinal tract but also have whole-body manifestations, including insulin resistance. Epigenetic mechanisms are amenable to both environmental and circulating factors and contribute to determining the T cell landscape. The recently identified participation of the gut microbiota in the remodeling of the epigenome of immune cells has triggered a paradigm shift in our understanding of the etiology of various inflammatory diseases and opened new paths toward therapeutic strategies. In this review, we provide an overview of the contribution of the Th17/Treg balance in the development and progression of inflammatory bowel diseases and metabolic diseases. We discuss the involvement of epigenetic mechanisms in the regulation of T cell function in the particular context of dysbiosis. Finally, we examine the potential for nutritional interventions affecting the gut microbiota to reshape the T cell epigenome and address the inflammatory component of various diseases.
Highlights
Immune homeostasis is a complex process involving a wide variety of key immunological players
Changes in the gut microbiota are intimately linked to significant alterations in T helper 17 (Th17)/Treg balance, potentially mediated by epigenetic mechanisms, and contributing to the development and establishment of inflammatory bowel disease (IBD), obesity, and type 2 diabetes (T2D), and possibly other chronic inflammatory conditions
Targeting such epigenetic changes through the use of histone deacetylase (HDAC) inhibitors and miRNA-based therapies has recently started to emerge as a novel therapeutic option in the context of inflammatory diseases [144]
Summary
Immune homeostasis is a complex process involving a wide variety of key immunological players. Serum levels of IL-22, another Th17-related cytokine, are significantly increased in IBD patients, an observation further recapitulated in a mouse model of colitis [47, 48] This excessive pro-inflammatory response results from a decreased differentiation and accumulation, as well as functional defects in Tregs in the inflamed tissues [49] or in peripheral blood of IBD patients with active disease [50]. The upregulation of these pro-inflammatory cytokines is correlated with a significant reduction in the levels of several immunosuppressive cytokines including TGF-β, IL-10, and IL-33 [41, 49]. Obesity is characterized by low-grade chronic inflammation with abnormal cytokine production and the activation of various inflammatory
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