Abstract
Inflammatory bowel disease (IBD) is an increasingly urgent medical problem that strongly impairs quality of life for patients. A global rise in incidence has been observed over the last few decades, with the highest incidence rates recorded in North America and Europe. Still, an increased incidence has been reported in the last ten years in newly industrialized countries in Asia, including China and India, both with more than one billion inhabitants. These data underline that IBD is an urgent global health problem. In addition, it is estimated that between 20% and 30% of IBD patients will develop colorectal cancer (CRC) within their lifetime and CRC mortality is approximately 50% amongst IBD patients. Although the exact etiology of IBD is still being defined, it is thought to be due to a complex interaction between many factors, including defects in the innate and adaptive immune system; microbial dysbiosis, i.e., abnormal levels of, or abnormal response to, the gastrointestinal microbiome; a genetic predisposition; and several environmental factors. At present, however, it is not fully understood which of these factors are the initiators of inflammation and which are compounders. The purpose of this review is to analyze the complex balance that exists between these elements to maintain intestinal homeostasis and prevent IBD or limit adverse effects on people’s health.
Highlights
A global rise in incidence of inflammatory bowel diseases (IBD) has been observed over the last decades, with the highest incidence rates recorded in high income countries
The dynamic crosstalk between intestinal epithelial cells (IECs), the microbiome, and immune cells is crucial for the maintenance of intestinal homeostasis [3]
Its breakdown can lead to the onset of inflammatory bowel diseases (IBD), chronic relapsing diseases characterized by intestinal inflammation, and epithelial damage, whicharise in genetically susceptible people exposed to environmental risk factors [4,5]
Summary
A global rise in incidence of IBD has been observed over the last decades, with the highest incidence rates recorded in high income countries. The etiology of IBD is still being defined, but many different genetic, immune, microbial, and environmental factors contribute, which is nutrition This latter factor probably exerts a more significant influence on IBD development: several studies have shown that a diet rich in proteins and unsaturated fats and low in fiber derived from fruits and vegetables can trigger a pro-inflammatory response in susceptible individuals [8]. Specific mutations of NOD2 (Arg702Trp, Gly908Arg, 1007fs) cause a defective binding with the muramyl dipeptide with consequent alteration of NF-κB activation This altered pathway increases the number of bacteria in the lumen, reduces elimination of pathogens, and inhibits the levels of antimicrobial peptides, such as defensins that allow the expression of NOD2 in Paneth cells. The G308A and C511T polymorphisms affect the TNFand IL-1β promoters, respectively, and cause an alteration in the production of these cytokines [19] Both CD and UC show activation of the humoral immune response. Th2 profile is expressed, it has been shown that UC has an atypical Th2 response mediated by IL-13 producing NK cells [23,24]
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