Airway chemosensitive receptors in vagus nerve perform neuro-immune interaction for lung-brain communication.
Recently, IL-1beta has been found to activate airway C-fiber receptors (CFRs) and high threshold Adelta receptors (HTARs), which may influence innate immune response via activation of the central nervous system. The present study aims to determine whether such a stimulatory effect is restricted to IL-1beta or applies to other pro-inflammatory cytokines. In anesthetized, open-chest, and mechanically ventilated rabbits, we recorded single unit activity from vagal nociceptors and examined their response to microinjection of TNF-alpha (1 microg/ml, 20 microl) directly into the receptive fields. Both CFRs and HTARs had similar responses. Their activity increased from 0.12+/-0.05 to 0.93+/-0.16 imp/s (n=15; P<0.001). This stimulatory effect of TNF-alpha was significantly attenuated by mixing with neutralizing antibody (10 microg/ml, 20 microl). The activities were 0.31+/-0.09 and 0.57+/-0.16 imp/s for control and injection of the TNF-alpha mixture (n=9; P<0.01), respectively. These nociceptors did not respond to location injection of normal saline. Our results show that TNF-alpha, like IL-1beta, can activate airway nociceptors. It lends support to the hypothesis that airway nociceptors in the lung mediate the innate immune response.
Li
H F
HF
Department of Pulmonary Medicine, University of Louisville, Louisville, KY 40292, USA, h0li0013@louisville.edu.
Yu
J
J
D000818:Animals; D001921:Brain / Q000502:physiology*; D016207:Cytokines / Q000008:administration & dosage / Q000276:immunology / Q000494:pharmacology; D007113:Immunity, Innate / Q000276:immunology; D018836:Inflammation Mediators / Q000008:administration & dosage / Q000276:immunology / Q000494:pharmacology; D008168:Lung / Q000276:immunology* / Q000294:innervation*; D015213:Neuroimmunomodulation; D009619:Nociceptors / Q000276:immunology*; D011817:Rabbits; D012018:Reflex / Q000276:immunology; D014630:Vagus Nerve / Q000378:metabolism*
D016207:Cytokines; D018836:Inflammation Mediators