|Kahl, Stanislaw - Stass|
|RHOADS, ROBERT - University Of Arizona|
|BAUMGARD, LANCE - University Of Arizona|
|COLLIER, ROBERT - University Of Arizona|
Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/21/2015
Publication Date: 7/1/2015
Citation: Kahl, S., Elsasser, T.H., Rhoads, R., Baumgard, L., Collier, R. 2015. Environmental heat stress modulates thyroid status and its response to repeated endotoxin challenge in steers. Domestic Animal Endocrinology. 52:43-50. doi: 10.1016/j.domaniend.2015.02.001. Epub 2015 Feb 26.
Interpretive Summary: Although mammals possess finely regulated mechanisms to control their internal temperature throughout a wide range of environmental temperatures, the imposition of high levels of ambient heat progressively tax the cellular use of energy. As more demands are put on the system to dispel the imbalances imposed by the heat, more and more resources are diverted from growth, lactation, and immune function just to stay alive. As the impact of heat stress progresses, animals often develop increased sensitivity to other health threats including those surrounding disease and infection. Few data address the nature of the mechanisms that are perturbed by such confounded health threats, heat and proinflammatory disease stress in particular. The thyroid axis in the body regulates and coordinates many aspects of energy use by cells, as well as the production of internal body heat necessary for thermoregulation. The present research addressed this heat and proinflammatory stress problem for cattle by systematically evaluating critical control points for regulation and function of the thyroid axis. Using a controlled growing dairy steer model of cycling daily heat changes between 32 and 40oC (environmental chambers) coupled with a double injection challenge of the bacteria-mimicking product endotoxin, we demonstrated that both the pituitary gland and the peripheral tissues themselves are critically impacted by heat and infection stress. The presence of heat stress alone significantly reduced the level of thyroid hormone activity under basal heat stress conditions. However, when the burden of an infection stress was added, perturbations in the fundamental basis for regulation and metabolic adjustment were observed. From this we conclude that not only is the thyroid axis perturbed by heat and infection stress, but by measuring components of this axis such as the thyroid hormones themselves, we can monitor the severity of the insult. This information is useful for developing means to cope with heat stress in livestock.
Technical Abstract: While the Holstein breed has been recognized as particularly sensitive to heat stress (HS), few data address the compounded dairy industry issue of responses to disease vectors in the face of HS. Thyroid hormones are important in the adaptation to HS, 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 HS stress and the response of this thyroid status to immune stress modeled by Gram negative bacterial endotoxin (LPS) challenge. Ten steers (318 ± 49 kg BW) housed in climate chambers were subjected to either a thermoneutral (TN: constant 19°C) environment or HS conditions (cyclical daily temperatures: 32.2 to 40.0°C) for 9 d. In order to minimize further 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; 0.2 µg/kg BW, intravenously, Escherichia Coli 055:B5) with jugular 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. Activity of 5’-deiodinase (D1) was estimated in liver biopsy samples collected before the LPS1 (0 h) and 24 h after the LPS2. 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. Repeated LPS challenge reduced (P < 0.01) hepatic activity of D1 in all animals but no differences were observed between steers subjected to TN or HS. 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.