Airway nociceptors activated by pro-inflammatory cytokines

Abstract The present studies evaluate whether the vagus nerves link the lungs’ immune and neural systems by transmitting information through pulmonary nociceptors. Single unit activities from pulmonary nociceptors [C fiber receptors (CFRs) and high threshold Aδ fiber receptors (HTARs)] were recorded...

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Bibliographic Details
Published in:Respiratory physiology & neurobiology 2007-05, Vol.156 (2), p.116-119
Main Authors: Yu, Jerry, Lin, Shuxin, Zhang, Jingwen, Otmishi, Peyman, Guardiola, Juan J
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
Inflammation
Interleukin
Interleukin-1beta - physiology
Laryngeal Nerves - physiology
Larynx - cytology
Larynx - immunology
Larynx - physiology
Male
Medical Education
Membrane Potentials - physiology
Nerve Fibers - physiology
Nerve Fibers, Unmyelinated - physiology
Neural immune interaction
Neuroimmunomodulation - physiology
Nociceptors - physiology
Pulmonary receptors
Pulmonary/Respiratory
Rabbits
Signal Transduction - physiology
Trachea - cytology
Trachea - immunology
Trachea - innervation
Trachea - physiology
Vagal afferents
Vagus Nerve - physiology
Vertebrates: respiratory system
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Summary:Abstract The present studies evaluate whether the vagus nerves link the lungs’ immune and neural systems by transmitting information through pulmonary nociceptors. Single unit activities from pulmonary nociceptors [C fiber receptors (CFRs) and high threshold Aδ fiber receptors (HTARs)] were recorded from the cervical vagus nerve in anesthetized, open-chest, and mechanically ventilated rabbits. Interleukin1β was then injected into the nociceptor field (IL-1β, 10 μg/ml, 20 μl). Both CFRs and HTARs were stimulated by the local injection; their activities increased from 0.2 ± 0.1 to 1.8 ± 0.5 imp/s ( n = 10; p < 0.01), and from 0.2 ± 0.1 to 1.1 ± 0.1 imp/s, respectively ( n = 6; p < 0.01). These increases were greatly attenuated by simultaneous administration of IL-1β with IL-1ra, a natural IL-1 receptor antagonist. The nociceptors were not stimulated by local injection of normal saline. Our data demonstrate that nociceptors can be activated by pro-inflammatory cytokines and support the hypothesis that airway nociceptors transmit immune signals from the lung to the brain.
ISSN:1569-9048
1878-1519
DOI:10.1016/j.resp.2006.11.005