Publications by authors named "Remzi O Eren"

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parasites block the activation of the inflammasome by inhibiting maturation of IL-1β.

Microb Cell 2018 Jan 14;5(3):137-149. Epub 2018 Jan 14.

Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.

The various symptomatic outcomes of cutaneous leishmaniasis relates to the type and potency of its underlying inflammatory responses. Presence of the cytoplasmic RNA virus-1 (LRV1) within , 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 infection irrespective of its LRV1-status. Further, neither LRV1-bearing (+) nor LRV1-negative () activated the inflammasome . Interestingly, similarly to , infection induced the up-regulation of the A20 protein, known to be involved in the evasion of inflammasome activation. Moreover, we observed that + 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 infection irrespective of the LRV1-status.
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http://dx.doi.org/10.15698/mic2018.03.619DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5826701PMC
January 2018