Molecular Genetics of Inflammatory Bowel Disease


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Tryptophan metabolites generated by the microbiota have been shown to be important in the mucosal immune response, and activation of the aryl hydrocarbon receptor AhR by tryptophan metabolites can direct the production of IL, a cytokine important in intestinal homeostasis.

Accordingly, supplementation with tryptophan-metabolizing Lactobacillus strains was sufficient to rescue susceptibility to colitis. These and other findings clearly show that innate immune sensors and response regulators, such as NOD2 and CARD9, respectively, limit the expansion of disease-promoting microorganisms in the gut, allowing beneficial microbes to thrive, and thus contribute to host health.

The close interaction between the host and the microbiota involves the shaping of the microbiota by the host and concurrent signaling from commensal microbes through immune-mediated recognition receptors to promote host tissue and immune development [ 2 ].

Gene–environment interactions in inflammatory bowel disease

Maintaining this bidirectional communication is critical for supporting intestinal homeostasis. Yet, defects in host signaling pathways may result in increased susceptibility to microbial infections while at the same time may disrupt the fundamental interactions with the indigenous commensal microbes.

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Indeed, genome-wide association studies GWAS have identified susceptibility genes involved in immune signaling pathways [ 1 ]. As described above, NOD2 is involved in bacterial sensing and pathogen surveillance during health and disease.


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Furthermore, NOD2 stimulation has been shown to activate autophagy, a conserved cellular pathway involved in the clearance of intracellular microbes [ 1 , 7 ]. Knockout mouse models for the genes Atg16l1 , Irgm , or Nod2 have all been reported to be impaired in pathogen clearance. Moreover, defects in ATG16L1 result in diminished secretion of antimicrobial peptides from abnormal Paneth cells and reduced antigen presentation—all features that may contribute to IBD pathogenesis [ 1 ]. In addition to the detection and clearance of intracellular pathogens, we recently revealed a role for ATG16L1 and NOD2 in sensing immunomodulatory commensal bacteria to promote tolerogenic immune responses to maintain intestinal homeostasis.

Mouse dendritic cells deficient in either Atg16l1 or Nod2 were unable to induce regulatory T-cell responses to suppress mucosal inflammation upon treatment with Bacteroides fragilis , both in vitro and during experimental colitis [ 10 ].


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Therefore, in addition to their role in bacterial clearance, we have proposed a complementary role for ATG16L1 and NOD2, in which these immune pathways also participate in the sensing of beneficial microbes [ 10 ]. Our work suggests that patients carrying risk alleles of IBD susceptibility genes may be cumulatively affected, first in sensing and clearance of intracellular microbes, and second in the recognition of immunomodulatory bacterial molecules from the gut microbiota to promote immune tolerance. Collectively, dysbiosis of the microbiome and the loss of beneficial commensal microbes, along with impairments in these IBD susceptibility genes, may lead to chronic, sustained mucosal inflammation, contributing to IBD pathogenesis.

While host genetics and the gut microbiome have separately been considered to be contributing factors to host health and disease in various immune-mediated pathologies, it is now clear that the synergism between these two players is key to our understanding of the pathogenesis of IBD. The intestinal microbial community has evolved alongside the host, contributing to immunity and energy metabolism [ 2 ]. Emerging studies have revealed that a more diverse microbiome and its microbial metabolites are important in maintaining intestinal homeostasis.

However, dysbiosis may result in a loss of microbial functional pathways important in the production of bacterial metabolites, such as tryptophan [ 9 ], short chain fatty acids SCFAs , and other compounds with anti-inflammatory activities to regulate intestinal inflammation [ 1 ]. Exploring gene—gut microbiome interactions may uncover novel strategies for early diagnosis and treatment of IBD. As probiotics and fecal microbiota transplant therapies become increasingly prevalent for IBD treatment, there is also a need to understand the mechanisms by which host immune pathways integrate microbiome-derived signals to promote intestinal homeostasis.

Understanding whether individuals carrying risk alleles associated with IBD are receptive to the beneficial effects of microbial therapies will facilitate personalized approaches to treatment. The implications of the microbiome on precision medicine may be an important consideration for treatment of IBD and other immune-mediated diseases.

In fact, recent studies have shown that the gut microbiome can predict patient responsiveness to immunomodulatory therapies, including both chemotherapies and an anti-integrin therapy vedolizumab used in IBD [ 11 ]. A personalized medicine approach that takes into consideration both host genetics and the gut microbiome could serve to predict therapeutic responses in the treatment of IBD and other immune-mediated diseases. Furthermore, future studies to identify novel pathways and their interactions with microbial communities could provide targets for more effective therapies and a better understanding of the pathogenesis of IBD.

Genetics and pathogenesis of inflammatory bowel disease. Chu H, Mazmanian SK.

From Inflammation to Cancer in Inflammatory Bowel Disease: Molecular Perspectives

Innate immune recognition of the microbiota promotes host-microbial symbiosis. Nat Immunol. Unravelling the effects of the environment and host genotype on the gut microbiome. Nat Rev Microbiol. Complex host genetics influence the microbiome in inflammatory bowel disease.

Host gene–microbiome interactions: molecular mechanisms in inflammatory bowel disease

Genome Med. Host genetic variation impacts microbiome composition across human body sites. Genome Biol. Human genetics shape the gut microbiome.

Nod2: the intestinal gate keeper. PLoS Pathog. Yan et al.

Jostins, L. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature , Mohanan, V.

www.cantinesanpancrazio.it/components/giqizig/22-comandare-luci-di.php

The molecular biology of inflammatory bowel diseases. - Abstract - Europe PMC

C1orf is a colitis risk gene that regulates stability of epithelial adherens junctions. Science , Rivas, M. Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease. Nature Genet. Yan, J. An inflammatory bowel disease-risk variant in INAVA decreases pattern recognition receptor-induced outcomes. NOTE: OMIM is intended for use primarily by physicians and other professionals concerned with genetic disorders, by genetics researchers, and by advanced students in science and medicine.

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Molecular Genetics of Inflammatory Bowel Disease Molecular Genetics of Inflammatory Bowel Disease
Molecular Genetics of Inflammatory Bowel Disease Molecular Genetics of Inflammatory Bowel Disease
Molecular Genetics of Inflammatory Bowel Disease Molecular Genetics of Inflammatory Bowel Disease
Molecular Genetics of Inflammatory Bowel Disease Molecular Genetics of Inflammatory Bowel Disease
Molecular Genetics of Inflammatory Bowel Disease Molecular Genetics of Inflammatory Bowel Disease
Molecular Genetics of Inflammatory Bowel Disease Molecular Genetics of Inflammatory Bowel Disease

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