Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases

Abstract

In this review, the role of innate and adaptive immunity in the pathogenesis of inflammatory bowel diseases (IBD) is reported. In IBD, an altered innate immunity is often found, with increased Th17 and decreased Treg cells infiltrating the intestinal mucosa. An associated increase in inflammatory cytokines, such as IL-1 and TNF-α, and a decrease in anti-inflammatory cytokines, such as IL-10, concur in favoring the persistent inflammation of the gut mucosa. Autoinflammation is highlighted with insights in the role of inflammasomes, which activation by exogenous or endogenous triggers might be favored by mutations of NOD and NLRP proteins. Autoimmunity mechanisms also take place in IBD pathogenesis and in this context of a persistent immune stimulation by bacterial antigens and antigens derived from intestinal cells degradation, the adaptive immune response takes place and results in antibodies and autoantibodies production, a frequent finding in these diseases. Inflammation, autoinflammation and autoimmunity concur in altering the mucus layer and enhancing intestinal permeability, which sustains the vicious cycle of further mucosal inflammation.

Crohn's disease and clinical management today: How it does?

“…Immunobiologicals have revolutionized the management of IBD by targeting the inflammatory processes associated with the disease, either by reducing pro-inflammatory cytokines or increasing regulatory cytokines[ 90 , 91 ]. British Society of Gastroenterology consensus guidelines recommend choosing a biological agent based on clinical factors, cost, safety, availability for use, as well as patient adherence and preference[ 92 ].…”

Geraniin Alleviates Inflammation in Caco-2 Cells and Dextran Sulfate Sodium-Induced Colitis Mice by Targeting IL-1β

“…1,2 The pathogenesis of these diseases is not yet fully understood; however, the imbalance between proinflammatory and regulatory cytokines is one of the main immunopathogenic causes contributing to the development of both these diseases. 5,6 Several cytokines, including TNF, IL-1β, and IL-6 are well-known important mediators of dysregulated inflammatory responses in patients with IBD. 7,8 Therefore, blocking the expression of these cytokines appears to be a promising approach for treating IBD, supported by the successful efficacy of anti-TNF biologics in patients with IBD.…”

“…Approximately 1.6 million U.S. residents and up to 2 million Europeans suffer from IBD, and recent reports suggest that the incidence is increasing in developing countries, including South America, Asia, Africa, and Eastern Europe . UC manifesting as inflammation mainly affects the colon mucosa, whereas CD can affect any part of the GI tract. , The pathogenesis of these diseases is not yet fully understood; however, the imbalance between proinflammatory and regulatory cytokines is one of the main immunopathogenic causes contributing to the development of both these diseases. , Several cytokines, including TNF, IL-1β, and IL-6 are well-known important mediators of dysregulated inflammatory responses in patients with IBD. , Therefore, blocking the expression of these cytokines appears to be a promising approach for treating IBD, supported by the successful efficacy of anti-TNF biologics in patients with IBD …”

Pharmacological Therapy in Inflammatory Bowel Diseases: A Narrative Review of the Past 90 Years

“…The interaction between the microbiota and the immune response (especially innate) is harmonious and self-limiting [ 3 ]. An imbalance that occurs in genetically prone individuals (genome), exposed to a propitious environment (interactome) causes the modification of the intestinal microbiota (microbiome) and an uncontrolled immune response (immunome) leading to the emergence of Ulcerative Colitis (UC) and Crohn’s Disease (CD): Inflammatory Bowel Diseases (IBD) [ 4 , 5 , 6 , 7 , 8 ].…”