Inflammatory and immunomodulatory mechanisms in the carotid body

Abstract

Evidence is available about the role of inflammatory/immunological factors in the physiology and plasticity of the carotid body, with potential clinical implications in obstructive sleep apnea syndrome and sudden infant death syndrome. In humans, lymphomonocytic aggregations (chronic carotid glomitis) have been reported in aging and opiate addiction. Glomus cells produce prostaglandin E2 and the cytokines interleukin 1β, interleukin 6 and TNF-α, with corresponding receptors. These factors modulate glomus cell excitability, catecholamine release and/or chemoreceptor discharge. The above cytokines are up-regulated in chronic sustained or intermittent hypoxia, and prevention of these changes, with ibuprofen or dexamethasone, may modulate hypoxia-induced changes in carotid body chemosensitivity. The main transcription factors considered to be involved are NF-kB and HIFs. Circulating immunogens (lipopolysaccharide) and cytokines may also affect peripheral arterial chemoreception, with the carotid body exerting an immunosensing function.