Rifampin resistance mutations in the rpoB gene of Enterococcus faecalis impact host macrophage cytokine production

Darya V. Urusova, Joseph A. Merriman, Ananya Gupta, Liang Chen, Barun Mathema, Michael G. Caparon, Shabaana A. Khader

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Antibiotic-resistant bacteria in the genus Enterococcus are a major cause of nosocomial infections and are an emergent public health concern. Similar to a number of bacterial species, resistance to the antibiotic rifampicin (RifR) in enterococci is associated with mutations in the gene encoding the β subunit of RNA polymerase (rpoB). In Mycobacterium tuberculosis, RifR rpoB mutations alter mycobacterial surface lipid expression and are associated with an altered IL-1 cytokine response in macrophages upon infection. However, it is not clear if RifR mutations modulate host cytokine responses by other bacteria. To address this question, we utilized Enterococcus faecalis (E. faecalis). Here, we treated human monocyte-derived macrophages with heat-inactivated wild type or RifR rpoB mutants of E. faecalis and found that RifR mutations reduced IL-1β cytokine production. However, RifR mutations elicited other potent pro- and anti-inflammatory responses, indicating that they can impact other immune pathways beyond IL-1R1 signaling. Our findings suggest that immunomodulation by mutations in rpoB may be conserved across diverse bacterial species and that subversion of IL-1R1 pathway is shared by RifR bacteria.

Original languageEnglish
Article number155788
StatePublished - Mar 2022


  • Enterococcus faecalis
  • IL-1β
  • Macrophage
  • Nosocomial infection
  • Rifampicin resistance mutation
  • rpoB gene


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