Abstract
Anemia is the main extra-gastrointestinal symptom in inflammatory bowel diseases (IBDs). Interleukin-6 (IL-6) and other cytokines are secreted and act in the microenvironment of the small intestine mucous membrane of IBD patients. Iron is essential for multiple cell functions and its homeostasis is regulated by the hepcidin–ferroportin axis. Hepcidin (HEPC) is mainly produced by the liver in response to iron needs but is also an acute phase protein. During inflammation, hepcidin is upregulated by IL-6 and is responsible for iron compartmentalization within cells, in turn causing anemia of inflammation. Tissues other than liver can produce hepcidin in response to inflammatory stimuli, in order to decrease iron efflux at a local level, then acting in an autocrine–paracrine manner. In IBDs and, in particular, in celiac disease (CeD), IL-6 might trigger the expression, upregulation and secretion of hepcidin in the small intestine, reducing iron efflux and exacerbating defective iron absorption. 7-Hydroxymatairesinol (7-HMR) belongs to the family of lignans, polyphenolic compounds produced by plants, and has nutraceutical antioxidant, anti-inflammatory and estrogenic properties. In this mini-review we revise the role of inflammation in IBDs and in particular in CeD, focusing our attention on the close link among inflammation, anemia and iron metabolism. We also briefly describe the anti-inflammatory and estrogenic activity of 7-HMR contained in foods that are often consumed by CeD patients. Finally, considering that HEPC expression is regulated by iron needs, inflammation and estrogens, we explored the hypothesis that 7-HMR consumption could ameliorate anemia in CeD using Caco-2 cells as bowel model. Further studies are needed to verify the regulation pathway through which 7-HMR may interfere with the local production of HEPC in bowel.
Highlights
The intestine has been defined as the most important lymphoid organ of the human body [1].the gut can suffer from different immune-mediated disorders like inflammatory bowel diseases (IBDs), including Crohn’s disease and ulcerative colitis, primary eosinophilic gastrointestinal disorders and celiac disease (CeD), which can alter both its structure and its functions
In IBDs and, in particular, in celiac disease (CeD), IL-6 might trigger the expression, upregulation and secretion of hepcidin in the small intestine, reducing iron efflux and exacerbating defective iron absorption. 7-Hydroxymatairesinol (7-HMR) belongs to the family of lignans, polyphenolic compounds produced by plants, and has nutraceutical antioxidant, anti-inflammatory and estrogenic properties. In this mini-review we revise the role of inflammation in IBDs and in particular in CeD, focusing our attention on the close link among inflammation, anemia and iron metabolism
We provide preliminary evidence that lignans could ameliorate inflammation and anemia in CeD, showing that lignans could inhibit the local expression of Interleukin-6 (IL-6) and hepcidin, the main regulator of iron homeostasis
Summary
The intestine has been defined as the most important lymphoid organ of the human body [1]. The gut can suffer from different immune-mediated disorders like inflammatory bowel diseases (IBDs), including Crohn’s disease and ulcerative colitis, primary eosinophilic gastrointestinal disorders and celiac disease (CeD), which can alter both its structure and its functions. In addition to the symptoms related to the gastrointestinal tract, extra-intestinal manifestations often occur in these disorders that complicate the whole clinical picture. Anemia is the most frequent extra-intestine clinical manifestation and contributes to worsening the quality of life of the patients affected by these pathologies [2]. Patients affected by CeD, one the main immune-mediated gastrointestinal disorders, present a high prevalence of anemia, ranging from 12% to 69% [3]. Anemia in CeD is mainly caused by malabsorption and iron deficiency, with the contribution of other micronutrient deficiencies, such as folate or vitamin B12 shortages [3].
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