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Peer-reviewedCC BYProceedings of the National Academy of Sciences of the United States of America

Myeloid cell reprogramming drives enhanced defense against Streptococcus pneumoniae lung infection following exposure to commensal Prevotella.

  • Sara N Stoner1
  • Eric D Larson2
  • Sam Fulte1
  • Steven C Shaw1
  • Erin R Fish1
  • Edward N Janoff3,4
  • Matthias Mack5
  • Sarah E Clark1
5 affiliations
  1. 1Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine, Aurora, CO 80045.
  2. 2Department of Basic and Translational Sciences, University of Pennsylvania School of Dental Medicine, Philadelphia, PA 19104.
  3. 3Division of Infectious Diseases, University of Colorado School of Medicine, Aurora, CO 80045.
  4. 4Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, CO 80045.
  5. 5Department of Nephrology, University Hospital Regensburg, Regensburg 93053, Germany.
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Abstract

Clinical data link the prevalent respiratory tract anaerobe Prevotella with reduced pneumonia mortality, but the mechanisms directing Prevotella regulation of lung immune homeostasis are unclear. Here, single-cell RNA sequencing was employed to define the transcriptional immune signatures underlying improved clearance of Streptococcus pneumoniae following lung exposure to Prevotella melaninogenica. Overall, we observed a substantial shift in myeloid cell transcriptional programming from interferon-dominant to a more antibacterial profile in S. pneumoniae-infected mice after pre-exposure to P. melaninogenica, correlating with increased macrophage and neutrophil phagocytosis of S. pneumoniae and improved pathogen clearance. In neutrophils, tumor necrosis factor (TNF) signaling through TNFR2 was essential for increased antimicrobial function. Moreover, improved defense required CCR2-dependent monocyte-derived macrophages, with selective enrichment of more a mature Cxcl3+ population which was distinct from the hallmark S. pneumoniae-associated C1qa+ population enriched in the absence of effective clearance. Together, these findings inform the myeloid cell transcriptional changes associated with natural infection resistance mediated by pulmonary microbial exposures.

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Cite

BibTeXRIS
BibTeX
@article{stoner2026myeloid,
  title = {{Myeloid cell reprogramming drives enhanced defense against Streptococcus pneumoniae lung infection following exposure to commensal Prevotella.}},
  author = {Sara N Stoner and Eric D Larson and Sam Fulte and Steven C Shaw and Erin R Fish and Edward N Janoff and Matthias Mack and Sarah E Clark},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  year = {2026},
  month = oct,
  doi = {10.1073/pnas.2623525123},
  url = {https://europepmc.org/article/MED/42842405},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Myeloid cell reprogramming drives enhanced defense against Streptococcus pneumoniae lung infection following exposure to commensal Prevotella.
AU  - Sara N Stoner
AU  - Eric D Larson
AU  - Sam Fulte
AU  - Steven C Shaw
AU  - Erin R Fish
AU  - Edward N Janoff
AU  - Matthias Mack
AU  - Sarah E Clark
PY  - 2026
DA  - 2026/10/07
JO  - Proceedings of the National Academy of Sciences of the United States of America
DO  - 10.1073/pnas.2623525123
UR  - https://europepmc.org/article/MED/42842405
AB  - Clinical data link the prevalent respiratory tract anaerobe Prevotella with reduced pneumonia mortality, but the mechanisms directing Prevotella regulation of lung immune homeostasis are unclear. Here, single-cell RNA sequencing was employed to define the transcriptional immune signatures underlying improved clearance of Streptococcus pneumoniae following lung exposure to Prevotella melaninogenica. Overall, we observed a substantial shift in myeloid cell transcriptional programming from interferon-dominant to a more antibacterial profile in S. pneumoniae-infected mice after pre-exposure to P. melaninogenica, correlating with increased macrophage and neutrophil phagocytosis of S. pneumoniae and improved pathogen clearance. In neutrophils, tumor necrosis factor (TNF) signaling through TNFR2 was essential for increased antimicrobial function. Moreover, improved defense required CCR2-dependent monocyte-derived macrophages, with selective enrichment of more a mature Cxcl3+ population which was distinct from the hallmark S. pneumoniae-associated C1qa+ population enriched in the absence of effective clearance. Together, these findings inform the myeloid cell transcriptional changes associated with natural infection resistance mediated by pulmonary microbial exposures.
SN  - 0027-8424
SN  - 1091-6490
ER  -