|Kahl, Stanislaw - Stass|
Submitted to: American Society for Experimental Biology and Medicine Proceedings
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/27/2000
Publication Date: N/A
Citation: N/A Interpretive Summary: An immune challenge (bacterial or viral infection, acute stress, or other nonpathogenic challenge) in food animals results in metabolic and endocrine shifts with decreased growth as an end result. During an immune challenge the body responds by producing or releasing compounds to the circulatory system that are called immune modulators. Tall fescue is the predominant cool season grass in the southeastern United States, most of it is infecte with an endophyte that produces ergot alkaloids which are considered to be the cause of fescue toxicosis in cattle which results in estimated production losses annually of over 600 million dollars. In an earlier study, when steers were grazing endophyte-infected tall fescue, there was an enhanced inflammatory response when steers were challenged by an endotoxin. In order to simulate the effect of grazing endophyte-infected tall fescue, in this study, steers were given acute doses of ergotamine tartrate. Results were quite different with an anti-inflammatory response suggesting that ergotamine tartrate may not mimic the effect of grazing toxic fescue or that an acute dose may be quite different than that resulting from chronic consumption in grazing cattle. The contrasting results suggest that further study is needed.
Technical Abstract: The objective of this study was to investigate whether the ergot alkaloid, ergotamine (ET), an alkaloid used to model fescue toxicosis in cattle, modifies the response of cattle to endotoxin (LPS) challenge. Steers (n=16) were divided into the following groups: control, ergotamine (ET), endotoxin (LPS), and ET+LPS. ET and ET+LPS groups received a single iv injection of ET (40 ug/kg of body weight), whereas C and LPS steers received a single injection of sterile vehicle. Thirty minutes after ET/vehicle administration, a single bolus iv injection of LPS (0.2 ug/kg body weight) was given. Blood was collected at various times for 48 hours. Endotoxin increased rectal temperature and circulating levels of tumor necrosis factor alpha, cortisol, haptoglobin (Hp), and thromboxane B2 (TXB2). Importantly, Hp, tumor necrosis factor alpha, and TXB2 increases were blunted by pretreatment with ET compared to LPS alone. Ergotamine by itself increased circulating cortisol, rectal temperature, plasma urea nitrogen and glucose, whereas it decreased serum prolactin. Thus, the acute dose of ET appeared to be anti-inflammatory as it decreased the inflammatory response to LPS, an effect likely driven at least in part by the ET-caused cortisol increase.