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Increasing evidence indicates that there exists a reciprocal communication between the immune system and the brain. Interleukin 1β (IL-1β), a proinflammatory cytokine produced during immune challenge, is believed to be one of the mediators of immune-to-brain communication, but how it gets into the brain is unknown because of its large molecular weight and difficulty in crossing the blood–brain barrier. Our previous work has demonstrated that IL-1 receptor type I is strongly expressed in the glomus cells of rat carotid body (CB), a well characterized polymodal chemoreceptive organ which serves not only for the detection of hypoxia, hypercapnia and acidity, but also for low temperature and blood glucose. The present study was designed to test whether IL-1β could stimulate the CB glomus cells and alter the discharge properties in the carotid sinus nerve, the afferent nerve innervating the organ. The results from whole-cell patch-clamp recordings and calcium imaging showed that extracellular application of IL-1β significantly decreased the outward potassium current and triggered a transient rise in [Ca2+]i in the cultured glomus cells of rat CB. Furthermore, by using extracellular recordings and pharmacological intervention, it was found that IL-1β stimulation of the CB in the anaesthetized rat in vivo significantly increased the discharge rate in the carotid sinus nerve, most probably mediated by ATP release. This experiment provides evidence that the CB responds to cytokine stimulation and proposes the possibility that the CB might play a role in immune-to-brain communication. [ABSTRACT FROM AUTHOR]

Abstract: Nicotine can increase size and severity of experimental choroidal neovascularization (CNV); however, the mechanism is uncertain. Recent studies demonstrated that the development of CNV involves the contribution of bone marrow-derived cells (BMCs). This study aims to investigate the effects and the potential mechanism of nicotine on BMCs'' contribution to CNV. Green fluorescent protein (GFP) chimeric mice were developed by transplanting bone marrow cells from GFP transgenic mice to C57BL/6J mice. CNV was induced by lasering. Nicotine was administered orally in drinking water. Histopathologic study and choroidal flatmount were performed to measure the CNV severity and BMCs recruitment. BMCs expressing different cell markers in CNV and local expressions of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and vascular cell adhesion molecule-1 (VCAM-1) were detected by immunofluorescence. Nicotine administration resulted in larger diameter and surface area of CNV (P <0.05). Nicotine-exposed mice demonstrated increased area and density of GFP+ cells, increased GFP+ vascular cells area, and decreased ratio of BMCs expressing F4/80 in CNV (P <0.05). Furthermore, the expression of VEGF and bFGF within CNV and VCAM-1 in choroid beneath CNV was up-regulated in nicotine-exposed mice. Our results suggest that nicotine promotes recruitment and incorporation of BMCs into CNV and affects differentiation of BMCs in CNV. These effects may be partly due to indirect actions of nicotine on BMCs via other factors (e.g. VEGF or VCAM-1). It is helpful to understand the mechanism of the effect of nicotine in CNV development. [Copyright &y& Elsevier]