Mechanisms of inflammasome signaling, microRNA induction and resolution of inflammation by helicobacter pylori

Beitrag in einem Sammelwerk
(Buchkapitel)


Details zur Publikation

Autorinnen und Autoren: Suneesh Kumar P, Blaser N, Backert S
Herausgeber: Steffen Backert
Titel Sammelwerk: Molecular Mechanisms of Inflammation: Induction, Resolution and Escape by Helicobacter pylori
Verlag: Springer Verlag
Jahr der Veröffentlichung: 2019
Titel der Reihe: Current Topics in Microbiology and Immunology
Band: 421
Seitenbereich: 267-302
ISSN: 0070-217X


Abstract

Inflammasome-controlled transcription and subsequent cleavage-mediated activation of mature IL-1β and IL-18 cytokines exemplify a crucial innate immune mechanism to combat intruding pathogens. Helicobacter pylori represents a predominant persistent infection in humans, affecting approximately half of the population worldwide, and is associated with the development of chronic gastritis, peptic ulcer disease, and gastric cancer. Studies in knockout mice have demonstrated that the pro-inflammatory cytokine IL-1β plays a central role in gastric tumorigenesis. Infection by H. pylori was recently reported to stimulate the inflammasome both in cells of the mouse and human immune systems. Using mouse models and in vitro cultured cell systems, the bacterial pathogenicity factors and molecular mechanisms of inflammasome activation have been analyzed. On the one hand, it appears that H. pylori-stimulated IL-1β production is triggered by engagement of the immune receptors TLR2 and NLRP3, and caspase-1. On the other hand, microRNA hsa-miR-223-3p is induced by the bacteria, which controls the expression of NLRP3. This regulating effect by H. pylori on microRNA expression was also described for more than 60 additionally identified microRNAs, indicating a prominent role for inflammatory and other responses. Besides TLR2, TLR9 becomes activated by H. pylori DNA and further TLR10 stimulated by the bacteria induce the secretion of IL-8 and TNF, respectively. Interestingly, TLR-dependent pathways can accelerate both pro- and anti-inflammatory responses during H. pylori infection. Balancing from a pro-inflammation to anti-inflammation phenotype results in a reduction in immune attack, allowing H. pylori to persistently colonize and to survive in the gastric niche. In this chapter, we will pinpoint the role of H. pylori in TLR- and NLRP3 inflammasome-dependent signaling together with the differential functions of pro- and anti-inflammatory cytokines. Moreover, the impact of microRNAs on H. pylori–host interaction will be discussed, and its role in resolution of infection versus chronic infection, as well as in gastric disease development.


FAU-Autorinnen und Autoren / FAU-Herausgeberinnen und Herausgeber

Backert, Steffen Prof. Dr.
Lehrstuhl für Mikrobiologie
Blaser, Nicole
Lehrstuhl für Mikrobiologie
Suneesh Kumar, Pachathundikandi, Ph.D.
Lehrstuhl für Mikrobiologie


Zitierweisen

APA:
Suneesh Kumar, P., Blaser, N., & Backert, S. (2019). Mechanisms of inflammasome signaling, microRNA induction and resolution of inflammation by helicobacter pylori. In Steffen Backert (Eds.), Molecular Mechanisms of Inflammation: Induction, Resolution and Escape by Helicobacter pylori. (pp. 267-302). Springer Verlag.

MLA:
Suneesh Kumar, Pachathundikandi, Nicole Blaser, and Steffen Backert. "Mechanisms of inflammasome signaling, microRNA induction and resolution of inflammation by helicobacter pylori." Molecular Mechanisms of Inflammation: Induction, Resolution and Escape by Helicobacter pylori. Ed. Steffen Backert, Springer Verlag, 2019. 267-302.

BibTeX: 

Zuletzt aktualisiert 2019-19-06 um 08:23