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Mycobacterium tuberculosis Limits Host Glycolysis and IL-1β by Restriction of PFK-M via MicroRNA-21

  • Emer E. Hackett
  • , Hugo Charles-Messance
  • , Seónadh M. O'Leary
  • , Laura E. Gleeson
  • , Natalia Muñoz-Wolf
  • , Sarah Case
  • , Anna Wedderburn
  • , Daniel G.W. Johnston
  • , Michelle A. Williams
  • , Alicia Smyth
  • , Mireille Ouimet
  • , Kathryn J. Moore
  • , Ed C. Lavelle
  • , Sinéad C. Corr
  • , Stephen V. Gordon
  • , Joseph Keane
  • , Frederick J. Sheedy
  • Trinity College Dublin
  • University College Dublin
  • New York University

Research output: Contribution to journalArticlepeer-review

Abstract

Hackett et al. identify a role for the anti-inflammatory miR-21 in limiting host glycolysis during tuberculosis (TB) infection to favor bacterial replication. This occurs by targeting a pro-glycolytic isoform at the rate-limiting step in glycolysis, PFK-M, a process antagonized by the host Th1-cytokine IFN-γ, to promote full macrophage activation and antimicrobial function.

Original languageEnglish
Pages (from-to)124-136.e4
JournalCell Reports
Volume30
Issue number1
DOIs
Publication statusPublished - 7 Jan 2020
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • glycolysis
  • interferon gamma
  • interleukin-1b
  • macrophage
  • metabolic reprogramming
  • microRNA
  • miR-21
  • mycobacterium tuberculosis
  • phosphofructokinase
  • tuberculosis

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