scholarly journals Reactive oxygen species production by human dendritic cells involves TLR2 and dectin-1 and is essential for efficient immune response against Mycobacteria

2016 ◽  
Vol 18 (6) ◽  
pp. 875-886 ◽  
Author(s):  
María Mercedes Romero ◽  
Juan Ignacio Basile ◽  
Laura Corra Feo ◽  
Beatriz López ◽  
Viviana Ritacco ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Immune Response ◽  
Dendritic Cells ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Efficient Immune Response ◽  
Human Dendritic Cells ◽  
Species Production

scholarly journals SHIP-1 Couples to the Dectin-1 hemITAM and Selectively Modulates Reactive Oxygen Species Production in Dendritic Cells in Response to Candida albicans

2015 ◽  
Vol 195 (9) ◽  
pp. 4466-4478 ◽  
Author(s):  
Noelia Blanco-Menéndez ◽  
Carlos del Fresno ◽  
Sandra Fernandes ◽  
Enrique Calvo ◽  
Ruth Conde-Garrosa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dendritic Cells ◽  
Candida Albicans ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Species Production

scholarly journals Ubiquitination of Listeria Virulence Factor InlC Contributes to the Host Response to Infection

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Edith Gouin ◽  
Damien Balestrino ◽  
Orhan Rasid ◽  
Marie-Anne Nahori ◽  
Véronique Villiers ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Immune Response ◽  
Listeria Monocytogenes ◽  
Host Response ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pathogenic Potential ◽  
Content Type ◽  
Species Production

ABSTRACT Listeria monocytogenes is a pathogenic bacterium causing potentially fatal foodborne infections in humans and animals. While the mechanisms used by Listeria to manipulate its host have been thoroughly characterized, how the host controls bacterial virulence factors remains to be extensively deciphered. Here, we found that the secreted Listeria virulence protein InlC is monoubiquitinated by the host cell machinery on K224, restricting infection. We show that the ubiquitinated form of InlC interacts with the intracellular alarmin S100A9, resulting in its stabilization and in increased reactive oxygen species production by neutrophils in infected mice. Collectively, our results suggest that posttranslational modification of InlC exacerbates the host response upon Listeria infection. IMPORTANCE The pathogenic potential of Listeria monocytogenes relies on the production of an arsenal of virulence determinants that have been extensively characterized, including surface and secreted proteins of the internalin family. We have previously shown that the Listeria secreted internalin InlC interacts with IκB kinase α to interfere with the host immune response (E. Gouin, M. Adib-Conquy, D. Balestrino, M.-A. Nahori, et al., Proc Natl Acad Sci USA, 107:17333–17338, 2010, https://doi.org/10.1073/pnas.1007765107). In the present work, we report that InlC is monoubiquitinated on K224 upon infection of cells and provide evidence that ubiquitinated InlC interacts with and stabilizes the alarmin S100A9, which is a critical regulator of the immune response and inflammatory processes. Additionally, we show that ubiquitination of InlC causes an increase in reactive oxygen species production by neutrophils in mice and restricts Listeria infection. These findings are the first to identify a posttranscriptional modification of an internalin contributing to host defense.

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