Literature DB >> 23689522

Inflammasomes in inflammatory bowel disease pathogenesis.

Ling-Yang Hao1, Xikui Liu, Luigi Franchi.   

Abstract

PURPOSE OF REVIEW: Inflammasomes are molecular platforms assembled in response to infection or danger signals, and they regulate the activation of caspase-1 and the maturation of the inflammatory cytokines IL-1β and IL-18. In this review, we will summarize the centrality of Nod-like receptor proteins that assemble inflammasomes and regulate intestinal homeostasis by controlling host defense responses, microbiota composition, intestinal inflammation and tissue damage. RECENT
FINDINGS: In the intestine, the innate immune system evolved to tolerate commensal microorganisms while maintaining the capacity to trigger host defense responses to invading pathogens. Recent findings suggest that inflammasomes play a critical role in the intricate interplay between the local microbial community and the mucosal immune system by sensing commensal bacteria, regulating microbial ecology, establishing the host defense response that discriminates pathogenic from commensal microbes and preventing the emergence of pathobionts. A model to reconcile the conflicting results in the literature on the role of inflammasomes in experimental colitis will be discussed.
SUMMARY: A better understanding of the relationship between inflammasome signaling and the intestinal microbiota might provide insight into the complex interaction of the innate immune system with the intestinal environment, and identify new approaches for the treatment of inflammatory bowel disease and gastrointestinal cancer.

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Year:  2013        PMID: 23689522     DOI: 10.1097/MOG.0b013e32836157a4

Source DB:  PubMed          Journal:  Curr Opin Gastroenterol        ISSN: 0267-1379            Impact factor:   3.287


  7 in total

1.  Differential expression of inflammasomes in lung cancer cell lines and tissues.

Authors:  Hui Kong; Yanli Wang; Xiaoning Zeng; Zailiang Wang; Hong Wang; Weiping Xie
Journal:  Tumour Biol       Date:  2015-04-25

2.  Endoplasmic Reticulum Stress Activates the Inflammasome via NLRP3- and Caspase-2-Driven Mitochondrial Damage.

Authors:  Denise N Bronner; Basel H Abuaita; Xiaoyun Chen; Katherine A Fitzgerald; Gabriel Nuñez; Yongqun He; Xiao-Ming Yin; Mary X D O'Riordan
Journal:  Immunity       Date:  2015-09-01       Impact factor: 31.745

3.  Cytosolic double-stranded RNA activates the NLRP3 inflammasome via MAVS-induced membrane permeabilization and K+ efflux.

Authors:  Luigi Franchi; Tatjana Eigenbrod; Raúl Muñoz-Planillo; Ulas Ozkurede; Yun-Gi Kim; Chakrabarti Arindam; Michael Gale; Robert H Silverman; Marco Colonna; Shizuo Akira; Gabriel Núñez
Journal:  J Immunol       Date:  2014-09-15       Impact factor: 5.422

4.  Vertically transmitted faecal IgA levels determine extra-chromosomal phenotypic variation.

Authors:  Clara Moon; Megan T Baldridge; Meghan A Wallace; Carey-Ann D; Herbert W Virgin; Thaddeus S Stappenbeck
Journal:  Nature       Date:  2015-02-16       Impact factor: 49.962

Review 5.  Modulation of inflammasome activity by Porphyromonas gingivalis in periodontitis and associated systemic diseases.

Authors:  Ingar Olsen; Özlem Yilmaz
Journal:  J Oral Microbiol       Date:  2016-02-04       Impact factor: 5.474

6.  Serum levels of NLRC4 and MCP-2/CCL8 in patients with active Crohn's disease.

Authors:  Kader Irak; Mehmet Bayram; Sami Cifci; Gulsen Sener
Journal:  PLoS One       Date:  2021-11-17       Impact factor: 3.240

7.  NLRP12 modulates host defense through IL-17A-CXCL1 axis.

Authors:  S Cai; S Batra; F Del Piero; S Jeyaseelan
Journal:  Mucosal Immunol       Date:  2015-09-09       Impact factor: 7.313

  7 in total

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