Nonpathogenic cutibacterium acnes confers host resistance against staphylococcus aureus

Ayano Tsuru, Yumi Hamazaki, Shuta Tomida, Mohammad Shaokat Ali, Tomomi Komura, Yoshikazu Nishikawa, Eriko Kage-Nakadai

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


Cutibacterium acnes is a human skin-resident bacterium. Although C. acnes maintains skin health by inhibiting invasion from pathogens like Staphylococcus aureus, it also contributes to several diseases, including acne. Studies suggest that differences in genetic background may explain the diverse phenotypes of C. acnes strains. In this study, we investigated the effects of C. acnes strains on the Caenorhabditis elegans life span and observed that some strains shortened the life span, whereas other strains, such as strain HL110PA4, did not alter it. Next, we assessed the effects of C. acnes HL110PA4 on host resistance against S. aureus. The survival time of C. acnes HL110PA4- fed wild-type animals was significantly longer than that of Escherichia coli OP50 control bacterium-fed worms upon infection with S. aureus. Although the survival times of worms harboring mutations at the daf-16/FoxO and skn-1/Nrf2 loci were similar to those of wild-type worms after S. aureus infection, administration of C. acnes failed to improve survival times of tir-1/SARM1, nsy-1/mitogen-activated protein kinase kinase kinase (MAPKKK), sek-1/mitogen-activated protein kinase kinase (MAPKK), and pmk-1/p38 mitogen-activated protein kinase (MAPK) mutants. These results suggest that the TIR-1 and p38 MAPK pathways are involved in conferring host resistance against S. aureus in a C. acnes-mediated manner.

Original languageEnglish
Article numbere00562-21
JournalMicrobiology spectrum
Issue number2
Publication statusPublished - Oct 2021


  • Caenorhabditis elegans
  • Cutibacterium acnes
  • P38 MAPK
  • Staphylococcus aureus
  • Tir-1

ASJC Scopus subject areas

  • Physiology
  • Ecology
  • Immunology and Microbiology(all)
  • Genetics
  • Microbiology (medical)
  • Cell Biology
  • Infectious Diseases


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