Author
Listed:
- Isaac M. Chiu
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Balthasar A. Heesters
(Boston Children’s Hospital, Program in Cellular and Molecular Medicine, and Harvard Medical School
Medical Microbiology, University Medical Center, Utrecht, Utrecht 3584 CX, The Netherlands)
- Nader Ghasemlou
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Christian A. Von Hehn
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Fan Zhao
(Quantitative Biology Program, Brandeis University)
- Johnathan Tran
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Brian Wainger
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Amanda Strominger
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Sriya Muralidharan
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
- Alexander R. Horswill
(Roy J. and Lucille A. Carver College of Medicine, University of Iowa)
- Juliane Bubeck Wardenburg
(University of Chicago)
- Sun Wook Hwang
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School
Korea University Graduate School of Medicine, Seoul 136-705, South Korea)
- Michael C. Carroll
(Boston Children’s Hospital, Program in Cellular and Molecular Medicine, and Harvard Medical School)
- Clifford J. Woolf
(Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School)
Abstract
Nociceptor sensory neurons are specialized to detect potentially damaging stimuli, protecting the organism by initiating the sensation of pain and eliciting defensive behaviours. Bacterial infections produce pain by unknown molecular mechanisms, although they are presumed to be secondary to immune activation. Here we demonstrate that bacteria directly activate nociceptors, and that the immune response mediated through TLR2, MyD88, T cells, B cells, and neutrophils and monocytes is not necessary for Staphylococcus aureus-induced pain in mice. Mechanical and thermal hyperalgesia in mice is correlated with live bacterial load rather than tissue swelling or immune activation. Bacteria induce calcium flux and action potentials in nociceptor neurons, in part via bacterial N-formylated peptides and the pore-forming toxin α-haemolysin, through distinct mechanisms. Specific ablation of Nav1.8-lineage neurons, which include nociceptors, abrogated pain during bacterial infection, but concurrently increased local immune infiltration and lymphadenopathy of the draining lymph node. Thus, bacterial pathogens produce pain by directly activating sensory neurons that modulate inflammation, an unsuspected role for the nervous system in host–pathogen interactions.
Suggested Citation
Isaac M. Chiu & Balthasar A. Heesters & Nader Ghasemlou & Christian A. Von Hehn & Fan Zhao & Johnathan Tran & Brian Wainger & Amanda Strominger & Sriya Muralidharan & Alexander R. Horswill & Juliane B, 2013.
"Bacteria activate sensory neurons that modulate pain and inflammation,"
Nature, Nature, vol. 501(7465), pages 52-57, September.
Handle:
RePEc:nat:nature:v:501:y:2013:i:7465:d:10.1038_nature12479
DOI: 10.1038/nature12479
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Cited by:
- Jonathan Madar & Namrata Tiwari & Cristina Smith & Divya Sharma & Shanwei Shen & Alsiddig Elmahdi & Liya Y. Qiao, 2023.
"Piezo2 regulates colonic mechanical sensitivity in a sex specific manner in mice,"
Nature Communications, Nature, vol. 14(1), pages 1-18, December.
- Min Jung & Michelle Dourado & James Maksymetz & Amanda Jacobson & Benjamin I. Laufer & Miriam Baca & Oded Foreman & David H. Hackos & Lorena Riol-Blanco & Joshua S. Kaminker, 2023.
"Cross-species transcriptomic atlas of dorsal root ganglia reveals species-specific programs for sensory function,"
Nature Communications, Nature, vol. 14(1), pages 1-15, December.
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