Vitamin A and inflammatory bowel diseases: from cellular studies and animal models to human disease

ABSTRACT

Introduction: Vitamin A (VA) and metabolites such as Retinoic Acid (RA) and all-trans-RA (at-RA) are crucial in the modulation of the immune system and may be determinative in the balance of the immune responses. Inflammatory bowel diseases (IBD) consist of chronic relapsing and heterogeneous disorders with not well-known etiology. Due to its role in inflammatory processes, VA may be helpful in the treatment of IBD.

Area covered: As VA plays a significant role in the inflammatory processes, this review aims to show the potential role of this vitamin in IBD, searching for cellular studies, animal models, and studies with humans.

Expert commentary: Many studies have described the importance of alternative therapeutic approaches for IBD. Due to its role in the immune system, VA may also exert an indispensable role in the IBD. Nevertheless, some authors have shown that these compounds could stimulate the release of pro-inflammatory cytokines. For these reasons, more studies should be performed to establish the precise mechanisms of VA and its metabolites in systemic and intestinal inflammation.

KEYWORDS:

• Inflammatory bowel disease
• vitamin A
• retinoic acid
• all-trans-retinoic acid

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Author contributions

S.M. Barbalho was responsible for the concept of the manuscript. S.M. Barbalho, R.A. Goulart, and G.L.S.A. Batista was responsible for the design and writing, and all contributed to and agreed on the final version of this review.

Additional information

Funding

This paper was not funded.