Hormone levels are associated with clinical markers and cytokine levels in hu‐ man localized cutaneous leishmaniasis
Gyselle Chrystina Baccan, Fabiano Oliveira, Adenilma Duranes Sousa, Natali Alexandrino Cerqueira, Jackson Mauricio Lopes Costa, Manoel Barral-Netto, Aldina Barral
Brain, Behavior, and Immunity
3 September 2010 1 December 2010 15 December 2010
Please cite this article as: Baccan, G.C., Oliveira, F., Sousa, A.D., Cerqueira, N.A., Costa, J.M.L., Barral-Netto, M., Barral, A., Hormone levels are associated with clinical markers and cytokine levels in human localized cutaneous leishmaniasis, Brain, Behavior, and Immunity (2010),
doi: 10.1016/j.bbi.2010.12.009 (aqui)
Abstract
Leishmaniasis is a serious health problem in several parts of the world, and localized cutaneous leishmaniasis (LCL) is the most frequent presentation of the tegumentary form of this disease cluster. Clinical presentations of leishmaniasis are influenced by both parasite and host factors, with emphasis on the host immune response. Alterations in plasma hormone levels have been described in many infections, and changes in hormone levels could be related to an imbalanced cytokine profile. In the present work, we evaluated a group of patients with LCL to determine changes in plasma hormone levels (cortisol, DHEA-S, estradiol, prolactin and testosterone) and their association with clinical markers of disease (lesion size, dose used to reach cure and time to cure) and with cytokines produced by PBMC stimulated by SLA (IFN-γ, IL-10 and TNF-α). Individuals with LCL exhibited lower plasma levels of DHEA-S, prolactin and testosterone compared with sex-matched controls, whereas levels of cortisol and estradiol were similar between patients and controls. Plasma levels of cortisol, estradiol or prolactin positively correlated with at least one clinical parameter. Cortisol and prolactin levels exhibited a negative correlation with levels of IFN-γ, whereas no correlation was observed with IL-10 or TNF-α levels. A decrease in DHEA-S levels was observed in male LCL patients when compared to male healthy controls. No other differences between the sexes were observed. Our results indicate a role for neuroendocrine regulation that restricts Th1 responses in human LCL. It is possible that, although impairing parasite killing, such neuroimmunomodulation may contribute to limiting tissue damage.
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