1. Mechanisms of Disease: Inflammatory Bowel Diseases
Guilherme Piovezani Ramos, MD, Konstantinos A. Papadakis, MD 
Mayo Clinic Proceedings 
Volume 94, Issue 1, Pages (January 2019)
DOI: /j.mayocp
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2. Figure 1
Mechanisms involved in the pathogenesis of inflammatory bowel disease (IBD). The pathogenesis of IBD is a result of the interplay between genetic, environmental, intestinal barrier, and immune response factors. GWAS = genome-wide association studies.
Mayo Clinic Proceedings  , DOI: ( /j.mayocp )
Copyright © 2018 Mayo Foundation for Medical Education and Research Terms and Conditions

3. Figure 2
The intestinal mucosa in the normal bowel and in inflammatory bowel disease (IBD). On exposure to environmental factors, patients with IBD have development of microbial dysbiosis with a decrease of short chain fatty acids (SCFA) producing bacteria and an increase in Proteobacteria. Mechanisms that maintain the intestinal barrier are also disrupted in the IBD mucosa, including down-regulation of epithelial cadherin (E-cadherin) in tight junctions; thickness of the mucus layer; abnormal goblet cell function, including mucin 2 (Muc2) and resistin-like molecule β (RELMβ) proteins; and dysfunctional Paneth cell–associated mechanisms, including secretion of antimicrobial products, nucleotide-binding oligomerization domain–containing protein 2 (NOD2), and autophagy-related 16-like 1 (ATG16L1) gene-associated functions. From the innate immune system perspective, the IBD mucosa has been found to exhibit a decrease in colonic macrophages expressing CD14, defective CX3CR1 (C-X3-C motif chemokine receptor 1) antigen presentation by dendritic cells; and impaired autophagy. Lastly, although leukocyte migration via integrin cellular adhesion molecule (CAM) interactions also occurs in the normal mucosa, the balance between effector and regulatory T cells (T-reg) appears to be disturbed in the IBD mucosa, resulting in uncontrolled activation of different T-cell lineages that migrate to the inflamed intestine. G = goblet cells; IFNγ = interferon γ; IL = interleukin; NK-T = natural killer T cell; P = Paneth cells; Th = T helper cell; TGFβ = tumor growth factor β; TNFα = tumor necrosis factor α.
Mayo Clinic Proceedings  , DOI: ( /j.mayocp )
Copyright © 2018 Mayo Foundation for Medical Education and Research Terms and Conditions

4. Mayo Clinic Proceedings 2019 94, 155-165DOI: (10. 1016/j. mayocp. 2018
Copyright © 2018 Mayo Foundation for Medical Education and Research Terms and Conditions