Dietary Component-Induced Inflammation and Its Amelioration by Prebiotics, Probiotics, and Synbiotics

Abstract

A balanced diet with many dietary components maintains immune homeostasis directly by interacting with innate and adaptive immune components or indirectly through gut microbiota and their metabolites. Dietary components may inhibit pro-inflammatory mediators and promote anti-inflammatory functions or vice versa. Western diets with imbalanced dietary components skew the immune balance toward pro-inflammation and induce intestinal inflammation, consequently leading to many intestinal and systemic inflammatory diseases like ulcerative colitis, Crohn's disease, irritable bowel syndrome, cardiovascular problems, obesity, and diabetes. The dietary component-induced inflammation is usually chronic in nature and frequently caused or accompanied by alterations in gut microbiota. Therefore, microbiome-targeted therapies such as probiotics, prebiotics and synbiotics hold great potentials to amend immune dysregulation and gut dysbiosis, preventing and treating intestinal and systemic inflammatory diseases. Probiotics, prebiotics and synbioitcs are progressively being added to foods and beverages, with claims of health benefits. However, the underlining mechanisms of these interventions for preventing and treating dietary component-induced inflammation are still not very clear. In addition, possibly ineffective or negative consequences of some probiotics, prebiotics and synbiotics call for stringent testing and regulation. Here, we will first briefly review inflammation, in terms of its types and the relationship between different dietary components and immune responses. Then, we focus on current knowledge about the direct and indirect effects of probiotics, prebiotics and synbiotics on intestinal and systemic inflammation. Understanding how probiotics, prebiotics and synbiotics modulate the immune system and gut microbiota will improve our strategies for preventing and treating dietary component-induced intestinal inflammation and inflammatory diseases.

Keywords: dysbiosis; inflammation; microbiota; prebiotics; probiotics; synbiotics; undernutrition; western diet.

FIGURE 1

Pictorial representation of the spectrum of inflammation where it is pathological inflammation at one extreme, and physiological inflammation at the other extreme (as part of normal homeostasis). In the middle of the spectrum is the dietary component-induced inflammation which is a special case that may lead to pathological or physiological inflammation.

FIGURE 2

Effects of microbiota on gut immune homeostasis. Gut microbiota and their metabolites interact with gut epithelial cells through PRR such as membranous Toll-like receptors and cytoplasmic NOD-like receptors. The subsequent inflammatory mediators activate other immune components. The gut immune system protects the epithelial lining and responds to incursions with different immune cells including dendritic cells, macrophages, CD4 and CD8 T cells and their cytokines like gamma interferon and IL-17 to proceed inflammation. IL-17 is important as it stimulates tight junction and mucin proteins and improves gut integrity and function. Longer and exaggerated inflammation is not helpful and counterproductive. Thus, T reg cells with the help of its key IL-10 cytokine control these cells and maintains immune homeostasis.

FIGURE 3

Potential anti-inflammatory mechanisms induced by probiotics, prebiotics and synbiotics. Probiotic, prebiotic and synbiotic can stimulate anti-inflammatory components of the immune system directly or indirectly through modulation of gut microbiota. These interventions interact with sentinel cells such as dendritic cells and macrophages through membrane receptors e.g., PRRs and suppress inflammation. Dendritic cells induce anti-inflammatory state through blocking transformation of naïve T cells into Th1 and Th17 cells and promote proliferation of Treg cells that consequently with help of their cytokines like IL-10 and TGF-β skew immune homeostasis toward anti-inflammatory state. Macrophages, once activated, produce different types of pro-inflammatory cytokines to promote inflammation but microbiota derived SCFA, especially butyrate, hinder different pathways like MAPK, STAT and NF-kB and suppress pro-inflammatory cytokines (monocyte chemotactic protein-1, TNF-α, and IL-12) from macrophages to suppress inflammation.

FIGURE 4

Overview of the impact of a balance diet versus western diet on gut microbiota and immune system and potential roles of interventions such as prebiotics, probiotics and synbiotics on microbiota-immune axis. In general, a balance diet modulates gut immune system directly or indirectly through gut microbiota with a mix of pro- and anti-inflammatory signals so that the immune system stays alert to keep its defenses but also remain tolerant to unnecessary signals to avoid needless inflammation (A). The pro-inflammatory components in western diet including low-quality fats (trans fatty acids and refined oils), refined carbohydrates (sugar and refined grains), unhealthy additives, processed red meat and salts directly modulate the immune system or negatively impact gut microbiota, causing dysbiosis and changes in metabolites leading to a leaky gut. Consequently, the gut immune homeostasis is shifted toward local or systemic chronic inflammation (B). Different interventions like prebiotics, probiotics and synbiotics can potentially amend dysbiosis and gut barrier integrity by promoting healthy gut microbiota and conferring their anti-inflammatory effects on immune system to restore gut immune homeostasis (C).