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Kulnik, S.

Publications and source records attributed to Kulnik, S..

2 recordsLinked to original sources

MINFLUX-nanoscopy of hNAIP/NLRC4 inflammasome activation in single human macrophages

The biochemical and structural basis of NAIP/NLRC4 inflammasome activation is well understood. Far less well known are the spatiotemporal processes within cells that play a role in the activation of the NAIP/NLRC4 inflammasome. We used super-resolution imaging technology, including MINFLUX nanoscopy, to investigate the human hNAIP/hNLRC4 inflammasome in primary human macrophages following the phagocytosis of a specific Yersinia enterocolitica strain. hNAIP, which senses components of the bacterial type III secretion system (T3SS) and activates NLRC4, was recruited to bacteria-containing phagosomes after they were disrupted by the T3SS. Disruption of a single phagosome within a macrophage was sufficient to cause the accumulation of NLRC4 and NLRP3 (a sensor of another inflammasome), as well as the adapter protein ASC, in a dense condensate known as a speck. This subsequently led to plasma membrane permeation and pyroptosis. It appeared that, with increasing infection time, clusters containing NLRC4 and NLRP3/NLRC4 gradually acquired ASC for speck formation. MINFLUX-nanoscopy was able to visualise hNAIP at disrupted phagosomes with nanometre resolution, and also revealed the number and organisation of NLRC4 inflammasome discs within a speck, as well as their hNAIP content, for the first time. Surprisingly, the number of NLRC4 inflammasome discs varied considerably, ranging from 35 to 249 per speck. Also, only a small fraction of these seemed to contain hNAIP. Our results significantly improve our understanding of the process by which the hNAIP/NLRC4 inflammasome is activated in macrophages that have ingested bacteria containing a T3SS.

cell biology↗

Immune activation of primary human macrophages is suppressed by the coordinated action of Yersinia effectors

In order to suppress the host immune response, numerous bacterial pathogens utilise a type 3 secretion system (T3SS) that injects effector proteins into host target cells. We investigated the T3SS effectors of Yersinia enterocolitica (Yops) for their individual and combined effects on gene expression, inflammasome formation and calcium signaling in primary human macrophages. YopP efficiently suppressed the up- and down-regulation of thousands of macrophage genes induced by the bacterias inflammatory stimuli. This was accompanied by parallel changes in histone 3-serine 10 phosphorylation, suggesting a higher-level regulatory mechanism. Surprisingly, YopM and YopQ counteracted selected YopP effects on gene expression, e.g., of cytokine pathways. A combination of YopP and YopQ, but not other combinations of Yops or any single Yop, reduced inflammasome formation. YopH alone blocked calcium transients in infected macrophages. We propose that the T3SS effectors of Yersinia antagonistically, synergistically or individually subdue major immune pathways of human macrophages to jointly suppress macrophage activation.

cell biology↗