Meeting Abstract
P1.214 Friday, Jan. 4 Effect of pre-hatch aromatase inhibition on post-hatch immunity in chickens (Gallus gallus) SIMKINS, JS*; BENOWITZ-FREDERICKS, ZM; KENNY, TC; Bucknell University; Bucknell University; Bucknell University jws049@bucknell.edu
Exposure to testosterone (“T”) during development can suppress immune function in many avian species. However, it is unclear whether this is caused by direct activation of androgen receptors. At least two lines of evidence suggest that estradiol (“E2”) is involved: E2 receptors are expressed on B- and T-lymphocytes and their progenitors, and E2 can inhibit lymphocyte production in vitro and in vivo. E2 is synthesized from T by the enzyme aromatase and this conversion is a necessary step in many T dependent signaling pathways. We hypothesized that immunosuppressive effects of in ovo T exposure are mediated by conversion to E2 by aromatase. To test this, we inhibited aromatization of endogenous T during a crucial period of pre-hatch immune system development and measured post-hatch immune activity (total IgY antibodies, response to PHA challenge, and size of thymus and bursa of Fabricius). On day 13 of incubation, when E2 receptor expression is at a maximum in bursal tissues, chicken eggs were injected with 0.1mg of the aromatase inhibitor fadrozole in saline or saline only. On day 14 post-hatch, chicks were injected in the wing web with 0.1mg of phytohemagglutinin (PHA) in PBS buffer. 24 hours later, swelling, an indicator of inflammation due to T-cell recruitment, was measured. Blood samples were taken on post-hatch day 3, day 13 (pre-PHA challenge), and day 15 (post-PHA challenge) and analyzed for total IgY antibody count. Thymus and bursa were weighed on day 16. We predicted that if immunomodulation by T were dependent on aromatization to E2, then fadrozole treatment would promote immune activity by inhibiting the pathway. Conversely, if T were acting on immune tissues directly by binding to androgen receptors, then fadrozole treatment would instead suppress immune activity by increasing T levels.
