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A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
Nonpathogenic Cutibacterium acnes Confers Host Resistance against Staphylococcus aureus
Ayano Tsuru1, Yumi Hamazaki1, Shuta Tomida2
1Graduate School of Human Life Science, Osaka City Universitygrid.261445.0, Osaka, Japan.
Cutibacterium acnes strains have varying effects on host health. Nonpathogenic strains, like HL110PA4, enhance host resistance against Staphylococcus aureus infection by activating specific immune pathways in model organisms.
Area of Science:
- Microbiology and Immunology
- Host-Microbe Interactions
- Model Organism Research (C. elegans)
Background:
- Cutibacterium acnes (C. acnes) is a common human skin bacterium with dual roles in health and disease.
- While C. acnes is linked to acne, its beneficial effects and strain-specific impacts on host immunity are less understood.
- Understanding C. acnes strain diversity is crucial for deciphering its role in the skin microbiome.
Purpose of the Study:
- To investigate the differential effects of C. acnes strains on the lifespan of the model organism Caenorhabditis elegans.
- To evaluate the protective role of a nonpathogenic C. acnes strain (HL110PA4) against Staphylococcus aureus infection.
- To elucidate the host immune pathways involved in C. acnes-mediated protection against S. aureus.
Main Methods:
- Assessed the impact of various C. acnes strains on C. elegans lifespan.
- Fed C. elegans with C. acnes HL110PA4 and subsequently infected them with S. aureus to measure survival rates.
- Utilized C. elegans mutants in key immune pathways (daf-16/FoxO, skn-1/Nrf2, tir-1/SARM1, nsy-1/MAPKKK, sek-1/MAPKK, pmk-1/MAPK) to identify mechanisms of protection.
Main Results:
- Certain C. acnes strains shortened C. elegans lifespan, while strain HL110PA4 did not affect it.
- C. elegans fed C. acnes HL110PA4 exhibited significantly increased survival upon S. aureus infection compared to controls.
- Host resistance mediated by C. acnes HL110PA4 against S. aureus required the TIR-1 and p38 MAPK pathways, but not DAF-16/FoxO or SKN-1/Nrf2.
Conclusions:
- C. acnes strains exhibit strain-specific pathogenicity and host interactions.
- Nonpathogenic C. acnes strains can confer significant host resistance against opportunistic bacterial infections.
- The TIR-1 and p38 MAPK signaling pathways are critical for C. acnes-mediated immune defense against S. aureus.
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