Neuroimmunological activation of the afferent laryngeal neural circuit in experimentally induced laryngeal inflammation.

CONCLUSIONS

These results show that laryngeal inflammatory reactions may induce the expression of proinflammatory cytokines along the afferent laryngeal circuit and in nuclei associated with the HPA axis. Local laryngeal inflammation may induce functional and physiologic alterations in the laryngeal neural system via neuroimmunologic reactions.

OBJECTIVE

Idiopathic laryngeal disorders associated with various neurologic conditions such as spasmodic dysphonia, idiopathic vocal fold paralysis and sudden infant death syndrome are causally related to upper respiratory tract infections, and it can be speculated that these disorders result in neurophysiologic alterations. The goal of this study was to identify the neurophysiologic effect on the central nervous system of local inflammatory alterations in the larynx.

MATERIAL AND

METHODS

The expression of c-fos and IL-1beta was identified after injecting saline solution, 10 microg of lipopolysaccharide or 100 microg of lipopolysaccharide into the larynx of 12 rats.

RESULTS

The inflammatory cytokine IL-1beta was mainly expressed in the inferior olivary nucleus and raphe nucleus, which are associated with the hypothalamic-pituitary-adrenal (HPA) axis. IL-1beta expression was also found in the nuclei of afferent nervous pathways of the superior laryngeal nerve, such as the nucleus tractus solitarius, nucleus ambiguus, lateral reticular nucleus, magnocellular reticular nucleus and paragigantocellular reticular nucleus.