Abstract
Intestinal inflammatory diseases, such as Crohn’s disease, ulcerative colitis, and necrotizing enterocolitis, are becoming increasingly prevalent. While knowledge of the pathogenesis of these related diseases is currently incomplete, each of these conditions is thought to involve a dysfunctional, or overstated, host immunological response to both bacteria and dietary antigens, resulting in unchecked intestinal inflammation and, often, alterations in the intestinal microbiome. This inflammation can result in an impaired intestinal barrier allowing for bacterial translocation, potentially resulting in systemic inflammation and, in severe cases, sepsis. Chronic inflammation of this nature, in the case of inflammatory bowel disease, can even spur cancer growth in the longer-term. Recent research has indicated certain natural products with anti-inflammatory properties, such as curcumin, can help tame the inflammation involved in intestinal inflammatory diseases, thus improving intestinal barrier function, and potentially, clinical outcomes. In this review, we explore the potential therapeutic properties of curcumin on intestinal inflammatory diseases, including its antimicrobial and immunomodulatory properties, as well as its potential to alter the intestinal microbiome. Curcumin may play a significant role in intestinal inflammatory disease treatment in the future, particularly as an adjuvant therapy.
Highlights
The incidence of intestinal inflammatory diseases, such as necrotizing enterocolitis (NEC), Crohn’s disease (CD), and ulcerative colitis (UC), is increasing worldwide
In an immune-mediated model of mouse colitis, Mouzaoui et al [321] demonstrated curcumin is capable of reducing neutrophil intestinal infiltration, thereby reducing MPO activity, as well as returning nitric oxide (NO) levels to baseline via inhibition of inducible nitric oxide synthase (iNOS) and reduced inflammatory cell infiltration
inflammatory bowel disease (IBD) and NEC are characterized by hyperstimulation of the immune system to luminal bacteria and dietary antigens, resulting in rampant intestinal inflammation
Summary
The incidence of intestinal inflammatory diseases, such as necrotizing enterocolitis (NEC), Crohn’s disease (CD), and ulcerative colitis (UC), is increasing worldwide. Ulcerative colitis, occasionally a milder condition, is characterized by continuous mucosal inflammation localized to the colon Both CD and UC result in extensive epithelial damage. IECs can sense microbes and microbial products, but they can respond by further reinforcement of their own physical barrier and coordination of the response by the intestinal immune system, becoming more or less tolerogenic as dictated by the intestinal luminal contents [11]. The functional immunological barrier of the intestines lies largely underneath the physical barrier of IECs. The immune system of the intestine is composed of both innate and adaptive arms. Innate immunity is comprised of primarily physical barriers (e.g., IEC mucus and AMP production), and a reactive component (e.g., resident and patrolling immune cells) [1]. The pathogenesis of intestinal inflammatory diseases likely involves both IECs and intestinal immune cells. The breakdown of the intestinal barrier is most often attributed to overproduction of pro-inflammatory cytokines, such as TNF-α, IL-1β, and interferon-gamma (IFN-γ) [7], triggered by activation of the nuclear factor-kappaB (NF-κB) and activator protein 1/mitogen-activated protein kinase (AP-1/MAPK) pathways
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
