Effect of neonatal capsaicin on peptide-containing primary afferent fibres, eosinophil distribution and hyperresponsiveness in rat lung tissue following experimentally induced eosinophilia.

Abstract

Treatment of neonatal rats with capsaicin causes a 92.4% loss of calcitonin-gene-related-peptide-immunoreactive unmyelinated sensory afferent fibres in the airways epithelium, vascular smooth muscle and perivascular adventitial layer of lung tissue compared with vehicle-treated controls. Rats were administered Sephadex particles i.v. 8-10 weeks after either capsaicin or vehicle treatment at birth in order to induce a granulomatous tissue inflammation, peripheral blood eosinophilia and pulmonary eosinophil invasion [Laycock et al., Int Arch Allergy Appl Immunol 1986;81:363-367]. The animals also exhibited lung hyperreactivity in vitro in response to carbachol and serotonin (5HT). In Sephadex-treated rats, capsaicin pretreatment did not affect the number of inflammatory cells in peripheral blood, the number of eosinophils in lung tissue, or the distribution of eosinophils in the adventitial tissue of blood vessels. Potencies of concentration-related contractures of lung tissue to 5HT and carbachol were increased by 50- to 100-fold in Sephadex-treated animals compared to controls, but in neither group was potency influenced by capsaicin pretreatment at birth. Recruitment and subsequent regional distribution of inflammatory cells in lung tissue and the increase in lung hyperresponsiveness exhibited in this model of asthma do not appear to involve neuropeptides released from primary afferent neurones.