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Peer-reviewedCC BY 4.0Nature Immunology

Microbial adhesion promotes Piezo1 activation to initiate innate immunity

  • Giulia Stucchi1
  • Marco Galli1
  • Stefano Cozzi1
  • Anna Celant1
  • Laura Marongiu1
  • Giuseppe Rocca1
  • Francesca Colnaghi1
  • Maria Rita Chelazzi1
  • Alessandra Polissi2
  • Alessandra Maria Martorana2
  • Giampiero Pietrocola3
  • Marina Vai1
6 more authors
  • Ivan Orlandi1
  • Renato Ostuni4
  • Simona Barresi4
  • Angelo Lombardo4,5
  • Metello Innocenti1
  • Francesca Granucci1
5 affiliations
  1. 1Department of Biotechnology and Biosciences, University of Milano-Bicocca, Piazza della Scienza 2, Milan, Italy
  2. 2Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy
  3. 3Dipartimento di Medicina Molecolare, Università degli Studi di Pavia, Pavia, Italy
  4. 4San Raffaele-Telethon Institute for Gene Therapy, IRCCS San Raffaele Scientific Institute, Milan, Italy
  5. 5Vita-Salute San Raffaele University, Milan, Italy
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Abstract

How mammals mount an effective immune response against infectious agents remains unresolved. Here we identify microbial adhesion to myeloid cells as a critical initiating event that precedes pattern recognition receptor (PRR) engagement. Using a skin infection model with pathogenic bacteria and fungi, we demonstrate that neutrophil recruitment occurs in two sequential phases. The early phase is PRR-independent and instead driven by microbial adhesion, which engages the mechanosensitive ion channel Piezo1 to promote leukotriene (LT)B4 production. Together with interleukin-1α, LTB4 induces CXCL1 release, triggering neutrophil infiltration via the same circuit at play during sterile inflammation. By contrast, the late phase is toll-like receptor (TLR)- and CXCL2-dependent, marking a transition to the canonical, pathogen-driven response. Our findings uncover microbial adhesion as a previously unrecognized danger signal that activates innate immunity via mechanotransduction, revealing a paradigm of how immune responses to infection are initiated.

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Cite

BibTeXRIS
BibTeX
@article{stucchi2026microbial,
  title = {{Microbial adhesion promotes Piezo1 activation to initiate innate immunity}},
  author = {Giulia Stucchi and Marco Galli and Stefano Cozzi and Anna Celant and Laura Marongiu and Giuseppe Rocca and Francesca Colnaghi and Maria Rita Chelazzi and Alessandra Polissi and Alessandra Maria Martorana and Giampiero Pietrocola and Marina Vai and Ivan Orlandi and Renato Ostuni and Simona Barresi and Angelo Lombardo and Metello Innocenti and Francesca Granucci},
  journal = {Nature Immunology},
  year = {2026},
  month = sep,
  doi = {10.1038/s41590-026-02643-y},
  url = {https://doi.org/10.1038/s41590-026-02643-y},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Microbial adhesion promotes Piezo1 activation to initiate innate immunity
AU  - Giulia Stucchi
AU  - Marco Galli
AU  - Stefano Cozzi
AU  - Anna Celant
AU  - Laura Marongiu
AU  - Giuseppe Rocca
AU  - Francesca Colnaghi
AU  - Maria Rita Chelazzi
AU  - Alessandra Polissi
AU  - Alessandra Maria Martorana
AU  - Giampiero Pietrocola
AU  - Marina Vai
AU  - Ivan Orlandi
AU  - Renato Ostuni
AU  - Simona Barresi
AU  - Angelo Lombardo
AU  - Metello Innocenti
AU  - Francesca Granucci
PY  - 2026
DA  - 2026/09/09
JO  - Nature Immunology
DO  - 10.1038/s41590-026-02643-y
UR  - https://doi.org/10.1038/s41590-026-02643-y
AB  - How mammals mount an effective immune response against infectious agents remains unresolved. Here we identify microbial adhesion to myeloid cells as a critical initiating event that precedes pattern recognition receptor (PRR) engagement. Using a skin infection model with pathogenic bacteria and fungi, we demonstrate that neutrophil recruitment occurs in two sequential phases. The early phase is PRR-independent and instead driven by microbial adhesion, which engages the mechanosensitive ion channel Piezo1 to promote leukotriene (LT)B4 production. Together with interleukin-1α, LTB4 induces CXCL1 release, triggering neutrophil infiltration via the same circuit at play during sterile inflammation. By contrast, the late phase is toll-like receptor (TLR)- and CXCL2-dependent, marking a transition to the canonical, pathogen-driven response. Our findings uncover microbial adhesion as a previously unrecognized danger signal that activates innate immunity via mechanotransduction, revealing a paradigm of how immune responses to infection are initiated.
SN  - 1529-2908
SN  - 1529-2916
ER  -