Nutrition, inflammation and liver-spleen axis

ABSTRACT

Chronic low-grade systemic inflammation represents a mechanism common to many diseases linked to atherosclerosis-related pathways. There is a growing body of evidence indicating that the combination of food quantity and quality along with genetic susceptibility are able to induce the aberrant activation of innate immune signalling, which initially contributes to chronic low-grade inflammation. Liver represents the central player to inflammatory response. Dietary/metabolic factors contribute to the pathogenesis of Non-alcoholic Fatty Liver Disease (NAFLD), the main causes of liver disease in the Western world. Enlargement of the spleen, central organ in regulating the inflammation-related immune response, is commonly seen in patients with of NAFLD, depicting the so called “liver-spleen axis.” The aim of this review was to provide an at-a-glance overview of the possible bi-directional mechanisms linking nutrition and inflammation, particularly pinpointing the inflammatory effects stemmed by nutrition on “liver-spleen axis.” In particular, the role of unhealthy diet, healthy dietary patterns, such as the Mediterranean diet style, dietary vitamins and micronutrients, such as vitamin D or Magnesium, and Glucagon-Like Peptide-1, a well-known incretin released in response to meal intake, will be discussed. The highly variability of the inflammatory response highlights the role of expert nutritionists in refining methodologies apt to assess nutritional epidemiology and to apply appropriate dietary intervention to counteract diet-induced inflammation mechanisms.

KEYWORDS:

• Diet
• Inflammation;
• Liver-spleen Axis;
• Nutrition
• Nutritionist

Disclosure statement

The authors have nothing to disclose. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author contributions

The authors' responsibilities were as follows: LB and SS: were responsible for the concept of this paper and drafted the manuscript; GM, GCT, FO, CDS and AC: provided a critical review of the paper. All authors contributed to and agreed on the final version of the manuscript.