2007
DOI: 10.4269/ajtmh.2007.76.1125
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17β-Estradiol INCREASES LEISHMANIA MEXICANA KILLING IN MACROPHAGES FROM DBA/2 MICE BY ENHANCING PRODUCTION OF NITRIC OXIDE BUT NOT PRO-INFLAMMATORY CYTOKINES

Abstract: We have previously shown that female DBA/2 mice are significantly more resistant to Leishmania mexicana compared with males. Here, we have analyzed the effect of 17beta-estradiol (E(2)) on function and cytokine production in male and female DBA/2 macrophages in vitro. We show that E(2) increases NO production and parasite killing in L. mexicana-infected male and female DBA/2 macrophages without increasing production of pro-inflammatory cytokines. These data indicate that E(2) may enhance leishmanicidal activit… Show more

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Cited by 30 publications
(41 citation statements)
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“…Infected male mice given intralesion IFN-c exhibited decreased lesion progression compared to control male mice (Satoskar et al 1998). The effects of sex steroid hormones is further evidenced by studies where estrogen treatment of bone marrow-derived macrophages from mice of both sexes demonstrated increased parasite killing and nitric oxide production without an increase in proinflammatory cytokines (Lezama-Davila et al 2007a).…”
Section: Parasitic Infectionsmentioning
confidence: 91%
“…Infected male mice given intralesion IFN-c exhibited decreased lesion progression compared to control male mice (Satoskar et al 1998). The effects of sex steroid hormones is further evidenced by studies where estrogen treatment of bone marrow-derived macrophages from mice of both sexes demonstrated increased parasite killing and nitric oxide production without an increase in proinflammatory cytokines (Lezama-Davila et al 2007a).…”
Section: Parasitic Infectionsmentioning
confidence: 91%
“…Finally, BMDMs were stained with Giemsa, and the infection rates, blinded by the number of parasites per 100 macrophages, were determined in triplicate. 58 …”
Section: Methodsmentioning
confidence: 99%
“…Both human and mouse monocytes and M/ express estrogen receptors (ERs) [23,25,26]. However, the effect of E2 on M/ depends on the cell, species, and cellular activation state [27], however, the consensus is that E2 usually biases the macrophage to produce non-inflammatory mediators, even during a parasitic infection [28]. The effect of P4 on M/ is less understood, mainly because M/ lack progesterone receptors (PR); however, M/ can still respond to P4 as P4 can act (with lower affinity) through the glucocorticoid receptor (GR) [29].…”
Section: Macrophagesmentioning
confidence: 99%