Alteration of immune function endpoints and differential expression of estrogen receptor isoforms in leukocytes from 17β-estradiol exposed rainbow trout (Oncorhynchus mykiss)

While the endocrine system is known to modulate immune function in vertebrates, the role of 17β-estradiol (E2) in cellular immune function of teleosts is poorly understood. The cellular and molecular responses of juvenile rainbow trout (Oncorhynchus mykiss) to E2 treatment were evaluated by exposing fish to 0.47 ± 0.02 μg/L E2 (mean ± SEM) for either 2 or 7 d, with a subsequent 14 d recovery period. After 2 and 7 d of exposure to E2, hematocrit was significantly lower than in control fish. Lipopolysaccharide-induced lymphocyte proliferation was elevated on day 2 and concanavalin A-induced lymphocyte proliferation was reduced following 7 d of E2 exposure. Four estrogen receptor (ER) transcripts were identified in purified trout head kidney leukocytes (HKL) and peripheral blood leukocytes (PBL). While the mRNA abundance of ERβ1 and ERβ2 was unaffected by treatment, ERα1 was up-regulated in HKL and PBL following 7 d of E2 exposure. ERα2 was up-regulated in HKL after 7 d of E2 exposure, but down-regulated in PBL after 2 and 7 d of treatment. All parameters that were altered during the E2 exposure period returned to baseline levels following the recovery period. This study reports the presence of the full repertoire of ERs in purified HKL for the first time, and demonstrates that ERα transcript abundance in leukocytes can be regulated by waterborne E2 exposure. It also demonstrated that physiologically-relevant concentrations of E2 can modulate several immune functions in salmonids, which may have widespread implications for xenoestrogen-associated immunotoxicity in feral fish populations inhabiting contaminated aquatic environments.

► We assessed effects of 17β-estradiol (E2) on the immune system of rainbow trout.
► Hematocrit and lymphocyte proliferation were altered by E2 treatment.
► Estrogen receptors were present in leukocytes and ERα was differentially regulated.
► All parameters returned to control levels within 14 d post-7d E2 exposure.
► At physiologically-relevant concentrations, E2 reversibly affects immune responses.