scholarly journals Role of Macrophage Scavenger Receptors in Response to Listeria monocytogenes Infection in Mice

2001 ◽  
Vol 158 (1) ◽  
pp. 179-188 ◽  
Author(s):  
Takuro Ishiguro ◽  
Makoto Naito ◽  
Takashi Yamamoto ◽  
Go Hasegawa ◽  
Fumitake Gejyo ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Scavenger Receptors ◽  
Listeria Monocytogenes Infection

scholarly journals The in vivo ISGylome links ISG15 to metabolic pathways and autophagy upon Listeria monocytogenes infection

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yifeng Zhang ◽  
Fabien Thery ◽  
Nicholas C. Wu ◽  
Emma K. Luhmann ◽  
Olivier Dussurget ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Metabolic Pathways ◽  
Quantitative Proteomics ◽  
Computational Analysis ◽  
Murine Models ◽  
Direct Modification ◽  
Catalytic Sites ◽  
Listeria Monocytogenes Infection

AbstractISG15 is an interferon-stimulated, ubiquitin-like protein, with anti-viral and anti-bacterial activity. Here, we map the endogenous in vivo ISGylome in the liver following Listeria monocytogenes infection by combining murine models of reduced or enhanced ISGylation with quantitative proteomics. Our method identifies 930 ISG15 sites in 434 proteins and also detects changes in the host ubiquitylome. The ISGylated targets are enriched in proteins which alter cellular metabolic processes, including upstream modulators of the catabolic and antibacterial pathway of autophagy. Computational analysis of substrate structures reveals that a number of ISG15 modifications occur at catalytic sites or dimerization interfaces of enzymes. Finally, we demonstrate that animals and cells with enhanced ISGylation have increased basal and infection-induced autophagy through the modification of mTOR, WIPI2, AMBRA1, and RAB7. Taken together, these findings ascribe a role of ISGylation to temporally reprogram organismal metabolism following infection through direct modification of a subset of enzymes in the liver.

scholarly journals CX3CR1+ CD115+ CD135+ common macrophage/DC precursors and the role of CX3CR1 in their response to inflammation

2009 ◽  
Vol 206 (3) ◽  
pp. 595-606 ◽  
Author(s):  
Cedric Auffray ◽  
Darin K. Fogg ◽  
Emilie Narni-Mancinelli ◽  
Brigitte Senechal ◽  
Celine Trouillet ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Dendritic Cell ◽  
Inflammatory Monocytes ◽  
Listeria Monocytogenes Infection ◽  
Plasmacytoid Dcs ◽  
Relationship Of ◽  
The Relationship ◽  
Cx3cr1 Expression

CX3CR1 expression is associated with the commitment of CSF-1R+ myeloid precursors to the macrophage/dendritic cell (DC) lineage. However, the relationship of the CSF-1R+ CX3CR1+ macrophage/DC precursor (MDP) with other DC precursors and the role of CX3CR1 in macrophage and DC development remain unclear. We show that MDPs give rise to conventional DCs (cDCs), plasmacytoid DCs (PDCs), and monocytes, including Gr1+ inflammatory monocytes that differentiate into TipDCs during infection. CX3CR1 deficiency selectively impairs the recruitment of blood Gr1+ monocytes in the spleen after transfer and during acute Listeria monocytogenes infection but does not affect the development of monocytes, cDCs, and PDCs.

scholarly journals The AP-1 transcription factors c-Jun and JunB are essential for CD8α conventional dendritic cell identity

2021 ◽  
Author(s):  
Philipp Novoszel ◽  
Barbara Drobits ◽  
Martin Holcmann ◽  
Cristiano De Sa Fernandes ◽  
Roland Tschismarov ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Listeria Monocytogenes ◽  
Dendritic Cell ◽  
Essential Role ◽  
Activator Protein 1 ◽  
Fate Specification ◽  
Cross Presentation ◽  
Listeria Monocytogenes Infection ◽  
And Function

AbstractDendritic cell (DC) development is orchestrated by lineage-determining transcription factors (TFs). Although, members of the activator-protein-1 (AP-1) family, including Batf3, have been implicated in conventional (c)DC specification, the role of Jun proteins is poorly understood. Here, we identified c-Jun and JunB as essential for cDC1 fate specification and function. In mice, Jun proteins regulate extrinsic and intrinsic pathways, which control CD8α cDC1 diversification, whereas CD103 cDC1 development is unaffected. The loss of c-Jun and JunB in DC progenitors diminishes the CD8α cDC1 pool and thus confers resistance to Listeria monocytogenes infection. Their absence in CD8α cDC1 results in impaired TLR triggering and antigen cross-presentation. Both TFs are required for the maintenance of the CD8α cDC1 subset and suppression of cDC2 identity on a transcriptional and phenotypic level. Taken together, these results demonstrate the essential role of c-Jun and JunB in CD8α cDC1 diversification, function, and maintenance of their identity.

scholarly journals Sex-Dependent Susceptibility to Listeria monocytogenes Infection Is Mediated by Differential Interleukin-10 Production

2005 ◽  
Vol 73 (9) ◽  
pp. 5952-5960 ◽  
Author(s):  
Bastian Pasche ◽  
Svetoslav Kalaydjiev ◽  
Tobias J. Franz ◽  
Elisabeth Kremmer ◽  
Valérie Gailus-Durner ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Inbred Mouse ◽  
Interleukin 10 ◽  
Mouse Strains ◽  
Opposite Pattern ◽  
Susceptibility To Infection ◽  
Listeria Monocytogenes Infection ◽  
Immunosuppressive Cytokine ◽  
Males And Females

ABSTRACT It is well documented that sex-dependent factors affect susceptibility to infection, with most mouse models demonstrating higher resistance in females. We made the unexpected observation that infection with the intracellular bacterium Listeria monocytogenes showed an opposite pattern in several commonly used inbred mouse strains: female C57BL/6J, BALB/c, C3H/HeN, and CBA/J mice were significantly more susceptible to Listeria infection. The pronounced sensitivity of females to Listeria, which was revealed by significantly higher lethality rates, correlated also with increased bacterial numbers in organ tissues (spleen and liver) and several immunological changes in peripheral blood samples. Surprisingly, increased severity of infection in females was associated with elevated interleukin-10 (IL-10) levels in plasma. Experiments using Il10 knockout mice, for which no differences between the susceptibilities of males and females to Listeria infection could be detected, confirmed the important role of this immunosuppressive cytokine for the outcome of disease. Our findings are likely to have clinical relevance, since similar sex differences with regard to infection with Listeria monocytogenes and other intracellular pathogens have been reported for humans.

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