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Review
. 2018 Aug 3;10(8):1016.
doi: 10.3390/nu10081016.

VSports手机版 - Retinoic Acid, Leaky Gut, and Autoimmune Diseases

Leila Abdelhamid  1 , Xin M Luo  2
Affiliations
Review

Retinoic Acid, Leaky Gut, and Autoimmune Diseases

Leila Abdelhamid et al. Nutrients. .

Abstract

A leaky gut has been observed in a number of autoimmune diseases including type 1 diabetes, multiple sclerosis, inflammatory bowel disease, and systemic lupus erythematosus. Previous studies from our laboratory have shown that lupus mice also bear a leaky gut and that the intestinal barrier function can be enhanced by gut colonization of probiotics such as Lactobacillus spp VSports手机版. Retinoic acid (RA) can increase the relative abundance of Lactobacillus spp. in the gut. Interestingly, RA has also been shown to strengthen the barrier function of epithelial cells in vitro and in the absence of probiotic bacteria. These reports bring up an interesting question of whether RA exerts protective effects on the intestinal barrier directly or through regulating the microbiota colonization. In this review, we will discuss the roles of RA in immunomodulation, recent literature on the involvement of a leaky gut in different autoimmune diseases, and how RA shapes the outcomes of these diseases. .

Keywords: autoimmune diseases; leaky gut; retinoic acid. V体育安卓版.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Retinoic acid (RA)-mediated cellular regulation in autoimmune diseases. RA suppresses the inflammatory T helper (Th)1/Th17 responses by decreasing interferon-γ (IFNγ) and interleukin (IL)-17. It also primes a regulatory/anti-inflammatory environment by enhancing IL-4, IL-10, IL-22, and transforming growth factor β (TGFβ). Through these mechanisms, RA may dampen different pathologies, including type 1 diabetes (T1D), multiple sclerosis (MS), and inflammatory bowel disease (IBD). However, the cellular mechanisms of RA in modulating systemic lupus erythematosus (SLE) are yet to be uncovered.
Figure 2
Figure 2
Possible mechanisms of how a leaky gut leads to autoimmunity. Breakdown of the integrity of the intestinal mucosa is associated with microbial dysbiosis. This could result in epigenetic changes of both self-protein and pattern recognition receptor (PRR) sensing. Increased danger signals following microbial dysbiosis provoke immunogenic cell responses, consequently upregulating different pro-inflammatory cytokines levels such as tumor necrosis factor (TNF)α, IFNγ, IL-1, IL-17, IL-6, and IL-13. These inflammatory niches are associated with different pathologies including IBD, MS, SLE, and T1D.
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