G., M.R., D.K. and R.H.]; and by the NIHR South London and Maudsley NHS Foundation selleck products Trust Specialist Biomedical Research Centre [to M.H.]. “
“Leishmaniasis comprises a cluster of diseases caused by different species of protozoa of the genus, Leishmania. Leishmaniasis is endemic in many areas of the world, including Brazil, and represents a serious public health problem ( WHO, 2007). In Brazil, localized cutaneous leishmaniasis
(LCL) is caused mainly by L. braziliensis and L. amazonensis ( Grimaldi et al., 1989). Protection is associated with the development of a T helper-1 (Th1) type cell-mediated immune response ( Alexander and Bryson, 2005). Neuroimmunomodulatory effects have been implicated in leishmaniasis. Stress, gender and age can influence disease outcome in mice and hamsters (Alexander, 1988, Travi et al., 2002, Ruiz et al., 2003 and Ehrchen et al., 2004), and selleck hormonal changes have been described in patients infected with L. mexicana ( Gallindo-Sevilla et al., 2007). Changes in plasma hormone levels have been correlated with an imbalanced cytokine profile in several acute and chronic infections ( Reincke et al., 1998, Bhasin et al., 2001, Leal et al., 2003, Leal et al., 2006,
Mavoungou et al., 2005, Libonati et al., 2006, Del Rey et al., 2007, Gallindo-Sevilla et al., 2007 and Pinto et al., 2007). Hormone level changes have also been implicated in the establishment of human malaria ( Kurtis et al., 2001). Stimulation of neuroendocrine axes, such as hypothalamus–pituitary–adrenal Digestive enzyme (HPA) and hypothalamus–pituitary–gonads (HPG) induces secretion of hormones which have profound effects on immune response (Besedovsky et al., 1986 and Webster et al., 2002). Glucocorticoids (GC) have been recognized as important immumodulators, promoting a shift from a Th1 to a Th2 cytokine response (Ramírez et al., 1996 and Ashwell et al., 2000). DHEA is a potential regulator of immune function and counteracts some effects of glucocorticoids (Hazeldine
et al., 2010). Estrogens can stimulate antibody production by B cells as well as production of IL-4 and IL-10 (Kanda and Tamaki, 1999, Janele et al., 2006 and Straub, 2007). Prolactin and testosterone also produce changes in immune system (Ansar et al., 1985, Olsen and Kovacs, 1996, Brand et al., 2004, Cutolo et al., 2004 and Dimitrov et al., 2004). In the present work, we studied a well-characterized group of male and female LCL patients to investigate hormonal changes in this infection. We also evaluated the relationship between plasma hormone levels and both clinical markers of disease and markers of the immune response. Patients included in this study (n = 57) were selected at the Centro de Referência Pirajá da Silva, Jequié (Bahia, Brazil), an endemic area for L. braziliensis ( de Oliveira et al., 2003).