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Peer-reviewedCC BYAnesthesiology and perioperative science

Microbial PAMPs-PRR driven neuroimmune signaling in the development of post-infectious persistent pain.

  • Ying Hong1
  • Gang Wang2
  • Mengmeng Zhou1
  • Yan Xu1
  • Hanbing Wang1
  • Mao Ye1
  • Xiao Xiao1
  • Li Zhou1
  • Guochang Hu3
  • Chunling Jiang1
  1. 1Department of Anesthesiology, The Research Units of West China (2018RU012), West China Hospital, Chinese Academy of Medical Sciences, Sichuan University, Chengdu, 610041 China.
  2. 2West China School of Medicine, Sichuan University, Chengdu, 610041 China.
  3. 3Departments of Anesthesiology and Pharmacology & Regenerative Medicine, University of Illinois College of Medicine, Chicago, Illinois USA.
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Abstract

Post-infectious persistent pain (PIPP) is a common long-term outcome of infection, but the link between transient infection and persistent pain remains unclear. Traditional explanations, such as tissue injury, residual inflammation, and nerve damage, do not fully explain pain persistence after pathogen clearance. This review proposes that signaling between pathogen-associated molecular patterns and pattern recognition receptors (PAMP-PRR) is a key mechanistic bridge from acute infection to persistent pain. Microbial ligands from bacterial, viral, fungal, and parasitic pathogens activate PRRs in immune cells, sensory neurons, glia, and epithelial cells, triggering shared neuroimmune programs that include inflammatory amplification, neuron-immune crosstalk, glial activation, and sensitization of peripheral and central pain pathways. Persistent microbial products, viral latency, repeated antigen exposure, and trained immunity may maintain these circuits and promote a shift from PAMP-driven responses to damage-associated molecular pattern (DAMP)-mediated sterile neuroinflammation. These observations reframe PIPP as a dynamic neuroimmune disorder and support biomarker-informed, stage-specific therapies aimed at restoring neuroimmune homeostasis while preserving host defense.Graphical abstract

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Cite

BibTeXRIS
BibTeX
@article{hong2026microbial,
  title = {{Microbial PAMPs-PRR driven neuroimmune signaling in the development of post-infectious persistent pain.}},
  author = {Ying Hong and Gang Wang and Mengmeng Zhou and Yan Xu and Hanbing Wang and Mao Ye and Xiao Xiao and Li Zhou and Guochang Hu and Chunling Jiang},
  journal = {Anesthesiology and perioperative science},
  year = {2026},
  month = oct,
  doi = {10.1007/s44254-026-00199-6},
  url = {https://europepmc.org/article/MED/42903367},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Microbial PAMPs-PRR driven neuroimmune signaling in the development of post-infectious persistent pain.
AU  - Ying Hong
AU  - Gang Wang
AU  - Mengmeng Zhou
AU  - Yan Xu
AU  - Hanbing Wang
AU  - Mao Ye
AU  - Xiao Xiao
AU  - Li Zhou
AU  - Guochang Hu
AU  - Chunling Jiang
PY  - 2026
DA  - 2026/10/19
JO  - Anesthesiology and perioperative science
DO  - 10.1007/s44254-026-00199-6
UR  - https://europepmc.org/article/MED/42903367
AB  - Post-infectious persistent pain (PIPP) is a common long-term outcome of infection, but the link between transient infection and persistent pain remains unclear. Traditional explanations, such as tissue injury, residual inflammation, and nerve damage, do not fully explain pain persistence after pathogen clearance. This review proposes that signaling between pathogen-associated molecular patterns and pattern recognition receptors (PAMP-PRR) is a key mechanistic bridge from acute infection to persistent pain. Microbial ligands from bacterial, viral, fungal, and parasitic pathogens activate PRRs in immune cells, sensory neurons, glia, and epithelial cells, triggering shared neuroimmune programs that include inflammatory amplification, neuron-immune crosstalk, glial activation, and sensitization of peripheral and central pain pathways. Persistent microbial products, viral latency, repeated antigen exposure, and trained immunity may maintain these circuits and promote a shift from PAMP-driven responses to damage-associated molecular pattern (DAMP)-mediated sterile neuroinflammation. These observations reframe PIPP as a dynamic neuroimmune disorder and support biomarker-informed, stage-specific therapies aimed at restoring neuroimmune homeostasis while preserving host defense.Graphical abstract
SN  - 2731-8389
ER  -