Current concept on the pathogenesis of inflammatory bowel disease-crosstalk between genetic and microbial factors: Pathogenic bacteria and altered bacterial sensing or changes in mucosal integrity take “toll”
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TL;DR: The genetic data acquired in recent years help in understanding the pathogenesis of IBD and can identify a number of potential targets for therapeutic intervention, and genetics may help more accurately diagnose and predict disease course in IBD.
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Abstract: The pathogenesis of inflammatory bowel disease (IBD) is only partially understood. Various environmental and host (e.g. genetic-, epithelial-, immune and non-immune) factors are involved. It is a multifactorial polygenic disease with probable genetic heterogeneity. Some genes are associated with IBD itself, while others increase the risk of ulcerative colitis (UC) or Crohn's disease (CD) or are associated with disease location and/or behaviour. This review addresses recent advances in the genetics of IBD. The article discusses the current information on the crosstalk between microbial and genetic factors (e.g. NOD2/CARD15, SLC22A46A5 and DLG5). The genetic data acquired in recent years help in understanding the pathogenesis of IBD and can identify a number of potential targets for therapeutic intervention. In the future, genetics may help more accurately diagnose and predict disease course in IBD.
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Peptidoglycan recognition proteins: modulators of the microbiome and inflammation
TL;DR: This Review analyses how one family of antibacterial pattern recognition molecules — the peptidoglycan recognition proteins — has evolved a fascinating variety of mechanisms to control host interactions with mutualistic, commensal and parasitic microorganisms to benefit both invertebrate and vertebrate hosts.
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Dietary polyphenols can modulate the intestinal inflammatory response.
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Has there been a change in the natural history of Crohn's disease? Surgical rates and medical management in a population-based inception cohort from Western Hungary between 1977-2009
Peter L. Lakatos,Petra A. Golovics,Gyula David,Tunde Pandur,Zsuzsanna Erdelyi,Agnes Horvath,Gabor Mester,Mihaly Balogh,Istvan Szipocs,C. Molnar,Erzsebet Komaromi,Gábor Veres,Barbara D. Lovasz,Miklós Szathmári,Lajos S. Kiss,Laszlo Lakatos +15 more
TL;DR: This population-based inception cohort has shown that the recent reduction in surgical rates was independently associated with increased and earlier AZA use and was significantly associated with the time to intestinal surgery in CD patients.
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Synergy between bacterial infection and genetic predisposition in intestinal dysplasia
TL;DR: This work shows that intestinal infection with Pseudomonas aeruginosa activates the c-Jun N-terminal kinase (JNK) pathway, a hallmark of the host stress response, and promotes a dramatic proliferation of SCs and progenitors that serves as a homeostatic compensatory mechanism to replenish the apoptotic enterocytes.
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TL;DR: It is reported here that B27 transgenic rats raised in a germfree environment do not develop inflammatory intestinal or peripheral joint disease, whereas the skin and genital inflammatory lesions are unaffected by the germfree state, and these findings support the concept that gut and joint inflammation are pathogenetically closely related.
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TL;DR: The mutational analyses of CARD15 in 453 patients with CD, including 166 sporadic and 287 familial cases, 159 patients with ulcerative colitis (UC), and 103 healthy control subjects provide tools for a DNA-based test of susceptibility and for genetic counseling in inflammatory bowel disease.
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TL;DR: Mdr1a/1b (-/-) mice should provide a useful model system to further test the pharmacological roles of the drug-transporting P-gps and to analyze the specificity and effectivity of P-gp-blocking drugs.
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