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Peer-reviewedCC BYEMBO Reports

Aurora A exacerbates antibiotic-resistant Staphylococcus aureus infection through ASC phosphorylation

  • Hajime Yamauchi1
  • Kei Sakamoto2
  • Yasuyuki Matsuda1
  • Yuko Tanishita3
  • Akito Ariyoshi2
  • Daisuke Sasaki4
  • Yu Shimoyama5
  • Akihiro Hasegawa5
  • Takayoshi Yamauchi1
  • Yoichiro Iwakura6
  • Haruki Okamura7
  • Shun’ichiro Taniguchi8
5 more authors
  • Masafumi Takahashi9
  • Akihiko Yoshimura3
  • Katsunori Yanagihara2
  • Gabriel Nuñez10
  • Hideki Hara1
10 affiliations
  1. 1Department of Infectious Diseases, Division of Microbiology and Immunochemistry, Asahikawa Medical University
  2. 2Department of Laboratory Medicine, Nagasaki University Graduate School of Biomedical Sciences
  3. 3Department of Microbiology and Immunology, Keio University School of Medicine
  4. 4Department of Laboratory Medicine, Nagasaki University Hospital
  5. 5Department of Microbiology and Immunology, Yamaguchi University Graduate School of Medicine
  6. 6Graduate School of Agricultural and Life Sciences, The University of Tokyo
  7. 7Laboratory of Tumor Immunology and Immunotherapy, Hyogo College of Medicine
  8. 8Department of Comprehensive Cancer Therapy, Shinshu University School of Medicine
  9. 9Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University
  10. 10Department of Pathology and Rogel Cancer Center, University of Michigan Medical School
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Abstract

Excessive inflammasome activation is increasingly recognized as a critical driver of pathology during bacterial infections, yet the pathogen-derived mechanisms that trigger dysregulated inflammasome responses remain poorly defined. Here, we identify a previously unrecognized role for the serine/threonine kinase Aurora A in promoting inflammasome activation during Staphylococcus aureus infection. We demonstrate that S. aureus activates JNK-dependent signaling in macrophages, leading to the phosphorylation of Aurora A. Activated Aurora A directly phosphorylates ASC, the inflammasome adaptor, on serine residues, enhancing ASC oligomerization and facilitating robust caspase-1 activation through both NLRP3 and AIM2 inflammasomes. This phosphorylation event stabilizes ASC speck formation and amplifies downstream IL-1β production, thereby intensifying inflammatory responses. Importantly, pharmacological inhibition or genetic disruption of Aurora A markedly suppresses inflammasome activation in vitro and in vivo, significantly reduces bacterial burdens and improves survival in mice infected with antibiotic-resistant S. aureus. These findings reveal Aurora A as a key host regulator exploited by S. aureus to potentiate inflammasome-driven inflammation and highlight inflammasome inhibition as a potential therapeutic strategy that augments host defense independently of antibiotic resistance.

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Cite

BibTeXRIS
BibTeX
@article{yamauchi2026aurora,
  title = {{Aurora A exacerbates antibiotic-resistant Staphylococcus aureus infection through ASC phosphorylation}},
  author = {Hajime Yamauchi and Kei Sakamoto and Yasuyuki Matsuda and Yuko Tanishita and Akito Ariyoshi and Daisuke Sasaki and Yu Shimoyama and Akihiro Hasegawa and Takayoshi Yamauchi and Yoichiro Iwakura and Haruki Okamura and Shun’ichiro Taniguchi and Masafumi Takahashi and Akihiko Yoshimura and Katsunori Yanagihara and Gabriel Nuñez and Hideki Hara},
  journal = {EMBO Reports},
  year = {2026},
  month = sep,
  doi = {10.1038/s44319-026-00918-x},
  url = {https://doi.org/10.1038/s44319-026-00918-x},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Aurora A exacerbates antibiotic-resistant Staphylococcus aureus infection through ASC phosphorylation
AU  - Hajime Yamauchi
AU  - Kei Sakamoto
AU  - Yasuyuki Matsuda
AU  - Yuko Tanishita
AU  - Akito Ariyoshi
AU  - Daisuke Sasaki
AU  - Yu Shimoyama
AU  - Akihiro Hasegawa
AU  - Takayoshi Yamauchi
AU  - Yoichiro Iwakura
AU  - Haruki Okamura
AU  - Shun’ichiro Taniguchi
AU  - Masafumi Takahashi
AU  - Akihiko Yoshimura
AU  - Katsunori Yanagihara
AU  - Gabriel Nuñez
AU  - Hideki Hara
PY  - 2026
DA  - 2026/09/01
JO  - EMBO Reports
DO  - 10.1038/s44319-026-00918-x
UR  - https://doi.org/10.1038/s44319-026-00918-x
AB  - Excessive inflammasome activation is increasingly recognized as a critical driver of pathology during bacterial infections, yet the pathogen-derived mechanisms that trigger dysregulated inflammasome responses remain poorly defined. Here, we identify a previously unrecognized role for the serine/threonine kinase Aurora A in promoting inflammasome activation during Staphylococcus aureus infection. We demonstrate that S. aureus activates JNK-dependent signaling in macrophages, leading to the phosphorylation of Aurora A. Activated Aurora A directly phosphorylates ASC, the inflammasome adaptor, on serine residues, enhancing ASC oligomerization and facilitating robust caspase-1 activation through both NLRP3 and AIM2 inflammasomes. This phosphorylation event stabilizes ASC speck formation and amplifies downstream IL-1β production, thereby intensifying inflammatory responses. Importantly, pharmacological inhibition or genetic disruption of Aurora A markedly suppresses inflammasome activation in vitro and in vivo, significantly reduces bacterial burdens and improves survival in mice infected with antibiotic-resistant S. aureus. These findings reveal Aurora A as a key host regulator exploited by S. aureus to potentiate inflammasome-driven inflammation and highlight inflammasome inhibition as a potential therapeutic strategy that augments host defense independently of antibiotic resistance.
SN  - 1469-3178
ER  -