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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Genomics and Improvement Laboratory » Research » Publications at this Location » Publication #291088
Title: Environmental heat stress modulates thyroid status and its response to repeated endotoxin (LPS) challenge in steers

Author
item Kahl, Stanislaw
item Elsasser, Theodore
item RHOADS, ROBERT - Virginia Polytechnic Institution & State University
item COLLIER, ROBERT - University Of Arizona
item BAUMGARD, LANCE - Iowa State University

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/17/2013
Publication Date: 6/15/2013
Citation: Kahl, S., Elsasser, T.H., Rhoads, R.P., Collier, R.J., Baumgard, L.H. 2013. Environmental heat stress modulates thyroid status and its response to repeated endotoxin (LPS) challenge in steers. J. Anim. Sci. 91: E-Suppl. 2, Program and Abstracts, 2013 pp. 481.

Interpretive Summary:

Technical Abstract: Thyroid hormones are important in the adaptation to heat stress, allowing the adjustment of metabolic rates in favor of decreased energy utilization and heat production. Thyroid status is compromised in a variety of acute and chronic infections and toxin-mediated disease states. Our objective was to evaluate in cattle, the activity of pituitary-thyroid axis during adaptation to heat stress and the response of this thyroid status to immune stress modeled by LPS challenge. Ten steers (318 ± 49 kg BW) housed in climate chambers were subjected to either a thermoneutral (TN: constant 19°C) environment or heat stress (HS) conditions (cyclical daily temperatures: 32.2 to 40.0°C) for 9 d. In order to minimize confounding effects of altered plane of nutrition, TN were pair-fed to HS. On d 4 and 7, steers received a LPS challenge (LPS1 and LPS2; E. Coli 055:B5, 0.2 µg/kg BW, i.v.) with blood samples collected at 0, 1, 2, 4, 7, and 24 h relative to the start of each challenge. Plasma concentrations of thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), and reverse-triiodothyronine (rT3) were measured by RIA. Before the start of LPS1, HS decreased (P < 0.01 vs. TN) plasma TSH (40%), T4 (45.4%), and T3 (25.9%), but did not affect rT3 concentrations. In TN group, LPS1 challenge decreased (P < 0.01 vs. 0 h) plasma concentrations of TSH between 1 and 7 h and T4 and T3 at 7 and 24 h. In HS steers, LPS1 injection reduced plasma TSH at 2 h only (P < 0.05), decreased plasma T3 at 7 and 24 h (P < 0.01) but did not affect already depressed plasma T4. In all steers, LPS1 increased (P < 0.01) plasma rT3 concentrations at 4, 7, and 24 h. The patterns of T4, T3, and rT3 changes during LPS2 were similar to those in LPS1 with less evident response in plasma TSH after LPS2. The data are consistent with the concept that HS adaptation in cattle results in the depression of pituitary-thyroid axis with preserved normal extrathyroidal T3 production. The data also suggest that LPS challenge suppresses both pituitary-thyroid axis and peripheral T3 generation, responses that are more apparent in steers subjected to previous HS exposure.