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Peer-reviewedCC BY-NC 4.0Journal of Innate Immunity

Functional divergence of regulatory and conventional bovine neutrophils following Mycobacterium bovis infection

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Abstract

Introduction: Bovine tuberculosis (bTB), due to Mycobacterium bovis (Mb) infection, is a chronic cattle disease and neglected cause of zoonotic tuberculosis. The role of neutrophils in bTB is overlooked. We recently identified a new neutrophil subset in cattle and mice with a similar morphology to conventional inflammatory neutrophils (Nconv). However, unlike Nconv, these regulatory neutrophils (Nreg) express MHC-II at their surface and can suppress lymphocyte proliferation. Methods: In this study, we compared the responses of bovine Nconv and Nreg to infection with a virulent Mb strain circulating in France and the attenuated Mb BCG vaccine. Results: Nreg and Nconv had different transcriptional profiles and were differentially activated by Mb infection. Both Nreg and Nconv efficiently killed Mb, but Nreg had higher levels of phagocytosis activity (2-fold difference) and ROS production (2.3-fold difference). Nreg had higher levels of mitochondrial activity and an ultrastructural organization different from that of Nconv. Conclusion: Our results provide the first insight into the functional characterization of bovine neutrophil subsets during Mb infection and highlight a new layer of complexity in their functional diversity that must be taken into account to improve our understanding of bTB pathophysiology, which is urgently required to improve the management of this costly disease.

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BibTeX
@article{saintvanne2026functional,
  title = {{Functional divergence of regulatory and conventional bovine neutrophils following Mycobacterium bovis infection}},
  author = {Maïa Saint-Vanne and Badreddine Bounab and Sebastien Eymieux and Emma Perdriau and Patricia Cunha and Florence Carerras and Romain Roullier and Yves Le Vern and Julien Pichon and Emilie Doz-Deblauwe and Pierre Germon and Nathalie Winter and Aude Remot},
  journal = {Journal of Innate Immunity},
  year = {2026},
  month = oct,
  doi = {10.1159/jin/adhag002},
  url = {https://hal.inrae.fr/hal-05793219v1},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Functional divergence of regulatory and conventional bovine neutrophils following Mycobacterium bovis infection
AU  - Maïa Saint-Vanne
AU  - Badreddine Bounab
AU  - Sebastien Eymieux
AU  - Emma Perdriau
AU  - Patricia Cunha
AU  - Florence Carerras
AU  - Romain Roullier
AU  - Yves Le Vern
AU  - Julien Pichon
AU  - Emilie Doz-Deblauwe
AU  - Pierre Germon
AU  - Nathalie Winter
AU  - Aude Remot
PY  - 2026
DA  - 2026/10/09
JO  - Journal of Innate Immunity
DO  - 10.1159/jin/adhag002
UR  - https://hal.inrae.fr/hal-05793219v1
AB  - Introduction: Bovine tuberculosis (bTB), due to Mycobacterium bovis (Mb) infection, is a chronic cattle disease and neglected cause of zoonotic tuberculosis. The role of neutrophils in bTB is overlooked. We recently identified a new neutrophil subset in cattle and mice with a similar morphology to conventional inflammatory neutrophils (Nconv). However, unlike Nconv, these regulatory neutrophils (Nreg) express MHC-II at their surface and can suppress lymphocyte proliferation. Methods: In this study, we compared the responses of bovine Nconv and Nreg to infection with a virulent Mb strain circulating in France and the attenuated Mb BCG vaccine. Results: Nreg and Nconv had different transcriptional profiles and were differentially activated by Mb infection. Both Nreg and Nconv efficiently killed Mb, but Nreg had higher levels of phagocytosis activity (2-fold difference) and ROS production (2.3-fold difference). Nreg had higher levels of mitochondrial activity and an ultrastructural organization different from that of Nconv. Conclusion: Our results provide the first insight into the functional characterization of bovine neutrophil subsets during Mb infection and highlight a new layer of complexity in their functional diversity that must be taken into account to improve our understanding of bTB pathophysiology, which is urgently required to improve the management of this costly disease.
SN  - 1662-811X
SN  - 1662-8128
ER  -