Peroxisome Proliferator-Activated Receptor γ Is Essential for the Resolution of Staphylococcus aureus Skin Infections

Cell Host Microbe. 2018 Aug 8;24(2):261-270.e4. doi: 10.1016/j.chom.2018.07.001. Epub 2018 Jul 26.

Abstract

Skin/soft tissue infections (SSTIs) caused by methicillin-resistant Staphylococcus aureus (MRSA) represent serious healthcare burdens worldwide. The host initially controls these infections with a pro-inflammatory infiltrate. However, once established, MRSA viability remains constant. To clear established MRSA SSTIs, the host must transition into the post-inflammatory resolution phase marked by infiltration of alternatively activated macrophages. Here we show that the host nuclear receptor, peroxisome proliferation activator receptor γ (PPARγ), is essential for this transition and MRSA clearance. Chemical PPARγ inhibition or genetic ablation of PPARγ in myeloid cells results in an extended inflammatory phase and exacerbated MRSA SSTIs. Conversely, treating mice with PPARγ agonists hastens the onset of the resolution phase and improves MRSA clearance in a myeloid-dependent fashion. The resolving fibrotic abscess lacks abundant glucose and oxygen but is replete with antimicrobial peptides, which together contribute to MRSA clearance. Thus, PPARγ agonists may serve as viable treatment options for complicated MRSA SSTIs.

Keywords: Staphylococcus aureus; infection resolution; macrophage polarization; nitric oxide; peroxisome proliferator receptor γ; polyamines; skin and soft tissue infection.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abscess / drug therapy
  • Abscess / etiology
  • Animals
  • Female
  • Glucose / metabolism
  • Host-Pathogen Interactions / physiology*
  • Male
  • Methicillin-Resistant Staphylococcus aureus / drug effects
  • Methicillin-Resistant Staphylococcus aureus / pathogenicity
  • Methicillin-Resistant Staphylococcus aureus / physiology
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • PPAR gamma / agonists
  • PPAR gamma / genetics
  • PPAR gamma / immunology*
  • PPAR gamma / metabolism
  • Rosiglitazone / pharmacology
  • Staphylococcal Skin Infections / drug therapy
  • Staphylococcal Skin Infections / etiology*

Substances

  • PPAR gamma
  • Rosiglitazone
  • Glucose