Corticosteroids inhibit Mycobacterium tuberculosis-induced necrotic host cell death by abrogating mitochondrial membrane permeability transition View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Jessica Gräb, Isabelle Suárez, Edeltraud van Gumpel, Sandra Winter, Fynn Schreiber, Anna Esser, Christoph Hölscher, Melanie Fritsch, Marc Herb, Michael Schramm, Laurens Wachsmuth, Christian Pallasch, Manolis Pasparakis, Hamid Kashkar, Jan Rybniker

ABSTRACT

Corticosteroids are host-directed drugs with proven beneficial effect on survival of tuberculosis (TB) patients, but their precise mechanisms of action in this disease remain largely unknown. Here we show that corticosteroids such as dexamethasone inhibit necrotic cell death of cells infected with Mycobacterium tuberculosis (Mtb) by facilitating mitogen-activated protein kinase phosphatase 1 (MKP-1)-dependent dephosphorylation of p38 MAPK. Characterization of infected mixed lineage kinase domain-like (MLKL) and tumor necrosis factor receptor 1 (TNFR1) knockout cells show that the underlying mechanism is independent from TNFα-signaling and necroptosis. Our results link corticosteroid function and p38 MAPK inhibition to abrogation of necrotic cell death mediated by mitochondrial membrane permeability transition, and open new avenues for research on novel host-directed therapies (HDT). More... »

PAGES

688

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-019-08405-9

    DOI

    http://dx.doi.org/10.1038/s41467-019-08405-9

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112023290

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30737374


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