ABSTRACT
Cutaneous leishmaniasis (CL) in mice has been shown to produce hyperalgesia and upregulation of interleukin (IL)-1beta and nerve growth factor (NGF) levels. The aim of this study was to investigate the effects of thymulin on CL-induced hyperalgesia and cytokine upregulation. Daily treatment with thymulin (1, 100, and 1000 ng/ip) produced dose-dependent decreases in CL-induced hyperalgesia as assessed by the tail flick and the hot plate tests. The levels of NGF and IL-1beta were determined in the skin tissues of the hind leg in different groups (n = 5 each) of mice over a period of 5 weeks. Mice with CL showed sustained increase in the levels of IL-1beta and NGF which were reversed by thymulin (1 microg). Injection of thymulin only did not alter the nociceptive thresholds or the levels of IL-1beta and NGF. We conclude that thymulin can modulate the hyperalgesia induced by CL by decreasing the levels of the proinflammatory factors IL-1beta and NGF.
Subject(s)
Hyperalgesia/drug therapy , Hyperalgesia/parasitology , Interleukin-1/metabolism , Leishmaniasis, Cutaneous/complications , Thymic Factor, Circulating/pharmacology , Animals , Dose-Response Relationship, Drug , Female , Mice , Mice, Inbred BALB C , Nerve Growth Factor/metabolism , Pain Threshold/drug effects , Up-Regulation/drug effects , Up-Regulation/immunologyABSTRACT
Classical description of syndromes produced by cutaneous leishmaniasis (CL) does not include sensory manifestations such as pain and/or itching, despite the evident upregulation of proinflammatory cytokines. Using a murine model of CL we report on evident hyperalgesia, as assessed by acute pain tests, and sustained upregulation of interleukin (IL-1beta) and nerve growth factor (NGF). This upregulation, especially that of NGF, may explain the observed hyperalgesia, in the light of recent evidence on the role of cytokines in the sensitization of nerve afferents and the subsequent hyperalgesia.
