Leishmania guyanensis parasites block the activation of the inflammasome by inhibiting maturation of IL-1β.
Details
Download: 2018A-Hartely-Microbial-Cell-Advanced-Pub-1.pdf (1774.92 [Ko])
State: Public
Version: Final published version
State: Public
Version: Final published version
Serval ID
serval:BIB_7AE1E45D5F8B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Leishmania guyanensis parasites block the activation of the inflammasome by inhibiting maturation of IL-1β.
Journal
Microbial Cell
ISSN
2311-2638 (Print)
ISSN-L
2311-2638
Publication state
Published
Issued date
2018
Peer-reviewed
Oui
Volume
5
Number
3
Pages
137-149
Language
english
Abstract
The various symptomatic outcomes of cutaneous leishmaniasis relates to the type and potency of its underlying inflammatory responses. Presence of the cytoplasmic javax.xml.bind.JAXBElement@52daeaa2 RNA virus-1 (LRV1) within javax.xml.bind.JAXBElement@be11ae5 , worsens lesional inflammation and parasite burden, as the viral dsRNA genome acts as a potent innate immunogen stimulating Toll-Like-Receptor-3 (TLR3). Here we investigated other innate pattern recognition receptors capable of reacting to dsRNA and potentially contributing to LRV1-mediated inflammatory pathology. We included the cytoplasmic dsRNA sensors, namely, the RIG-like receptors (RLRs) and the inflammasome-dependent and -independent Nod-like-receptors (NLRs). Our study found no role for RLRs or inflammasome-dependent NLRs in the pathology of javax.xml.bind.JAXBElement@3dfe8dc4 infection irrespective of its LRV1-status. Further, neither LRV1-bearing javax.xml.bind.JAXBElement@6e03fdb4 ( javax.xml.bind.JAXBElement@6b89952c +) nor LRV1-negative javax.xml.bind.JAXBElement@68bc8c8a ( javax.xml.bind.JAXBElement@2165acf4 ) activated the inflammasome javax.xml.bind.JAXBElement@507a0b31 . Interestingly, similarly to javax.xml.bind.JAXBElement@77fdd4e7 , javax.xml.bind.JAXBElement@7b29ce4e infection induced the up-regulation of the A20 protein, known to be involved in the evasion of inflammasome activation. Moreover, we observed that javax.xml.bind.JAXBElement@77a7dfd3 + promoted the transcription of inflammasome-independent NLRC2 (also called NOD2) and NLRC5. However, only NLRC2 showed some contribution to LRV1-dependent pathology. These data confirmed that the endosomal TLR3 pathway is the dominant route of LRV1-dependent signalling, thus excluding the cytosolic and inflammasome pathways. We postulate that avoidance of the inflammasome pathways is likely an important mechanism of virulence in javax.xml.bind.JAXBElement@77047195 infection irrespective of the LRV1-status.
Keywords
Leishmania, Leishmania-virus, metastatic leishmaniasis, inflammasome, NOD-like receptors, RIG-like receptors, A20
Pubmed
Open Access
Yes
Create date
15/01/2018 15:03
Last modification date
20/08/2019 15:36