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Title

The nuclear receptor LXR limits bacterial infection of host macrophages through a mechanism that impacts cellular NAD metabolism

AuthorsMatalonga, Jonathan; Glaria, Estibaliz; Bresque, Marina; Escande, Carlos; Carbó, José María; Kiefer, Kerstin; Vicente, Ruben; León, Theresa E.; Beceiro, Susana; Pascual-García, Mónica; Serret, Joan; Sanjurjo, Lucía; Morón-Ros, Samantha; Riera, Antoni; Paytubi, Sonia; Juarez, Antonio; Sotillo, fernando; Lindbom, Lennart; Caelles, Carme; Sarrias, Maria-Rosa; Sancho, Jaime; Castrillo, Antonio ; Chini, Eduardo N.; Valledor, Annabel F.
KeywordsMacrophage
Nuclear
Receptor
LXR
Bacterial
Infection
NAD
Cytoskeleton
CD38
Issue Date31-Jan-2017
PublisherElsevier
CitationCell Reports 18(5): 1241–1255 (2017)
AbstractMacrophages exert potent effector functions against invading microorganisms but constitute, paradoxically, a preferential niche for many bacterial strains to replicate. Using a model of infection by Salmonella Typhimurium, we have identified a molecular mechanism regulated by the nuclear receptor LXR that limits infection of host macrophages through transcriptional activation of the multifunctional enzyme CD38. LXR agonists reduced the intracellular levels of NAD+ in a CD38-dependent manner, counteracting pathogen-induced changes in macrophage morphology and the distribution of the F-actin cytoskeleton and reducing the capability of non-opsonized Salmonella to infect macrophages. Remarkably, pharmacological treatment with an LXR agonist ameliorated clinical signs associated with Salmonella infection in vivo, and these effects were dependent on CD38 expression in bone-marrow-derived cells. Altogether, this work reveals an unappreciated role for CD38 in bacterial-host cell interaction that can be pharmacologically exploited by activation of the LXR pathway.
Publisher version (URL)http://dx.doi.org/10.1016/j.celrep.2017.01.007
URIhttp://hdl.handle.net/10261/144470
DOI10.1016/j.celrep.2017.01.007
ISSN2211-1247
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(IPBLN) Artículos
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