Artigo de Periódico
Hormone levels are associated with clinical markers and cytokine levels in human localized cutaneous leishmaniasis
Fecha
2011Registro en:
1090-2139
v. 25.
Autor
Baccan, Gyselle Chrystina
Oliveira, Fabiano
Sousa, Adenilma Duranes
Cerqueira, Natali Alexandrino
Costa, Jackson Mauricio Lopes
Barral-Netto, Manoel
Barral, Aldina Maria Prado
Baccan, Gyselle Chrystina
Oliveira, Fabiano
Sousa, Adenilma Duranes
Cerqueira, Natali Alexandrino
Costa, Jackson Mauricio Lopes
Barral-Netto, Manoel
Barral, Aldina Maria Prado
Institución
Resumen
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-c, IL-10 and TNF-a). 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-c, whereas no correlation was observed with IL-10 or TNF-a 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 neuroimmuno-modulation may contribute to limiting tissue damage.