Ubiquitination as an Efficient Molecular Strategy Employed in Salmonella Infection

Narayanan, Lakshmi; Edelmann, Mariola J.

doi:10.3389/fimmu.2014.00558

Cited by 27 publications

(27 citation statements)

References 61 publications

(77 reference statements)

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“…Although di-Gly proteomics cannot distinguish between ubiquitin-and ISG15-modified peptides, our results corroborate those of Radoshevich et al and strongly suggest that L. monocytogenes uniquely interacts with the ER. Interestingly, despite good coverage of ubiquitylated peptides, we observed the fewest number of ubiquitylation changes during S. Typhimurium infection, consistent with the notion that this pathogen directly antagonizes the ubiquitin system extensively (Narayanan and Edelmann, 2014). During M. tuberculosis infection, sites with increased ubiquitylation were enriched in proteins that shape the phagosome environment, including multiple components of the vacuolar ATPase that functions to acidify the phagosome lumen (ATP6V0D1, ATP6V1H, ATP6V1B2).…”

Section: Global Ubiquitylation Analysis Reveals Common Host Pathways supporting

confidence: 80%

Comparative analysis of macrophage post-translational modifications during intracellular bacterial pathogen infection

Johnson¹,

Parry

Repasy

et al. 2020

Preprint

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SUMMARYMacrophages activate robust antimicrobial functions upon engulfing virulent bacteria, yet a wide array of pathogens paradoxically thrive within these innate immune cells. To probe the pathogen-macrophage interface, we used proteomics to comprehensively quantify changes in post-translational modifications (PTMs) of host proteins during infection with three evolutionarily diverse intracellular pathogens: Mycobacterium tuberculosis, Salmonella enterica serovar Typhimurium, and Listeria monocytogenes. Comparing global phosphorylation and ubiquitylation patterns identified extensive reprogramming of cellular pathways during infection, with ubiquitylation patterns revealing unique pathogen-specific molecular response signatures undetectable by transcriptional profiling. Differential PTM changes during infection with attenuated M. tuberculosis cells lacking the ESX-1 virulence determinant revealed extensive modification of phagosome dynamics and antiviral type I interferon activation. We found that M. tuberculosis-mediated activation of the antiviral OASL1-IRF7 pathway promotes bacterial replication, uncovering a new mechanism of virus-bacterial synergy. Our data reveals remarkable specificity in innate cellular responses to complex stimuli and provides a resource for deeper understanding of host-pathogen interactions.

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Section: Global Ubiquitylation Analysis Reveals Common Host Pathways supporting

confidence: 80%

Comparative analysis of macrophage post-translational modifications during intracellular bacterial pathogen infection

Johnson¹,

Parry

Repasy

et al. 2020

Preprint

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“…28 Autophagy machinery is recruited to these sites by CALCOCO2, SQSTM1, OPTN, and CALCOCO3, the latter a CALCOCO2 paralog. 23,30,31 In fibroblasts, we were unable to detect ubiquitin in the LGP C aggregate. Moreover, while in epithelial cells S. Typhimurium uses deubiquitinases like SseL to limit selective autophagy against ALIS, 59 our study in fibroblasts shows that the pathogen translocates SseL but that this SPI2 effector is not responsible for the lack of ubiquitin in the LGP C aggregate.…”

Section: Discussionmentioning

confidence: 63%

“…28 Ubiquitinated components on the pathogen surface and LGALS8 act as danger sensors recognized by diverse autophagy receptors, including CALCOCO2/NDP52, SQSTM1/p62, OPTN/optineurin and CALCOCO3/TAX1BP1. 23,[29][30][31] Diacylglycerol (DAG) signaling can also target S. Typhimurium to xenophagy. 32 These xenophagy events occur at early stages of the infection, 1 to 2 h after bacterial invasion of the epithelial cell.…”

Section: Introductionmentioning

confidence: 99%

Intracellular Salmonella induces aggrephagy of host endomembranes in persistent infections

et al. 2016

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Xenophagy has been studied in epithelial cells infected with Salmonella enterica serovar Typhimurium (S. Typhimurium). Distinct autophagy receptors target this pathogen to degradation after interacting with ubiquitin on the surface of cytosolic bacteria, and the phagophore-and autophagosome-associated protein MAP1LC3/LC3. Glycans exposed in damaged phagosomal membranes and diacylglycerol accumulation in the phagosomal membrane also trigger S. Typhimurium xenophagy. How these responses control intraphagosomal and cytosolic bacteria remains poorly understood. Here, we examined S. Typhimurium interaction with autophagy in fibroblasts, in which the pathogen displays limited growth and does not escape into the cytosol. Live-cell imaging microscopy revealed that S. Typhimurium recruits late endosomal or lysosomal compartments that evolve into a membranous aggregate connected to the phagosome. Active dynamics and integrity of the phagosomal membrane are requisite to induce such aggregates. This membranous structure increases over time to become an aggresome that engages autophagy machinery at late infection times (> 6 h postentry). The newly formed autophagosome harbors LC3 and the autophagy receptor SQSTM1/p62 but is devoid of ubiquitin and the receptor CALCOCO2/NDP52. Live-cell imaging showed that this autophagosome captures and digests within the same vacuole the aggresome and some apposed intraphagosomal bacteria. Other phagosomes move away from the aggresome and avoid destruction. Thus, host endomembrane accumulation resulting from activity of intracellular S. Typhimurium stimulates a novel type of aggrephagy that acts independently of ubiquitin and CALCOCO2, and destroys only a few bacteria. Such selective degradation might allow the pathogen to reduce its progeny and, as a consequence, to establish persistent infections.

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“…Small leucine-rich proteoglcan (SlrP) promotes cell death by facilitating the ubiquitylation of thioredoxin under ubiquitin ligase (Narayanan and Edelmann, 2014;Lin and Machner, 2017). This process depletes the thioredoxin level in the host cell and makes a cell vulnerable to oxidative damage and lead to apoptosis.…”

Section: Salmonella Survival In the Expense Of Host Cell Deathmentioning

confidence: 99%

Mechanisms for Salmonella Infection and Potential Management Options in Chicken

2020

THE JAPS

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Salmonella enterica is the largest species in genus Salmonella with its serovars responsible for infection in chickens and other warm-blooded hosts. After oral ingestion, Salmonella penetrates the mucosal layer of the gastrointestinal tract (GIT). It then provokes gastroenteritis and systemic infection to chickens of all ages depending on the serovar involved. The paper explains about Salmonella infection via Type Three Secretion System (TTSS) encoded Pathogenicity Islands (PIs) and how the bacterium survives the acidic environment of GIT. It also explains the roles of TTSS-1 and TTSS-2 in translocation of effectors that interfere with host proteins and later internalisation of Salmonella in Salmonellacontaining vacuole (SCV). Other virulence factors such as plasmid, biofilm and lipopolysaccharides are highlighted, and their importance in inducing pathogenicity to host was also included in the paper. Therefore, several factors are geared toward survival, infection, and replication of Salmonella in the host cells. Hence, this article explains the mechanisms of Salmonella infection in chicken, its persistence in different environments and the approaches in controlling chicken salmonellosis.

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Ubiquitination as an Efficient Molecular Strategy Employed in Salmonella Infection

Cited by 27 publications

References 61 publications

Comparative analysis of macrophage post-translational modifications during intracellular bacterial pathogen infection

Comparative analysis of macrophage post-translational modifications during intracellular bacterial pathogen infection

Intracellular Salmonella induces aggrephagy of host endomembranes in persistent infections

Mechanisms for Salmonella Infection and Potential Management Options in Chicken

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