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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 #316242

Title: Effects of lipopolysaccharide (LPS) induced inflammatory response on early embryo survival in ewes

Author
item GRAHAM, M - West Virginia University
item BOWDRIDGE, ELIZABETH - West Virginia University
item BOWDRIDGE, SCOTT - West Virginia University
item HOLASKOVA, IDA - West Virginia University
item Elsasser, Theodore
item DAILEY, ROBERT - West Virginia University

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/19/2015
Publication Date: 7/12/2015
Citation: Graham, M.R., Bowdridge, E.C., Bowdridge, S.A., Holaskova, I., Elsasser, T.H., Dailey, R.A. 2015. Effects of lipopolysaccharide (LPS) induced inflammatory response on early embryo survival in ewes. Meeting Abstract. 149.

Interpretive Summary:

Technical Abstract: Early pregnant ewes were used to determine the effects of endogenous (through LPS activation) and exogenous TNF-alpha tumor necrosis factor-alpha (TNF-alpha) on embryonic loss. Thirty-eight Dorset x Texel ewes were synchronized for estrus and bred to fertile rams (d0). On d5/6, ewes were assigned to receive via the jugular 2.5 mL containing either PBS (n=9), 2.5 microgram/kg LPS (n=9), 1 microgram/kg TNF-alpha (n=10) at 0 and 30min, or 2.5 microgram/kg of LPS after 3.5 mL containing 0.14 mg/kg BW im Dexamethasone (Dex, n=10) at -12 and 0h. Behavioral changes and rectal temperatures (BT) were recorded before challenge and hourly for 12h. Jugular blood was collected before challenge, every 30min for 3h, hourly until 12h, and at 24, 36, and 48h for TNF-alpha, and Hp and on d9/10 and 25/26 for progesterone. White blood cells were differentiated by staining. At d25/26, pregnancy was examined using ultrasonography. Treatment with LPS resulted in elevated BT for 6 hr, increased lethargy, mucosal response, white blood cell count, serum Hp concentrations, serum TNF-alpha, and greater embryonic loss compared to controls (p < 0.05). Treatment with LPS + Dex also had elevated BT for 6 hr, but was blunted by DEX. Additionally, Dex blocked mucosal and lethargic responses and attenuated LPS-induced increases in TNF-alpha. However, it did not improve embryonic survival compared to LPS alone (p > 0.05). The TNF-alpha treatment increased BT for 1h; however, high concentrations of TNF-alpha were not sustained. Thus, TNF-alpha did not induce lethargy; half the ewes showed a mucosal response; and white blood cell counts did not change. More control and TNF-alpha ewes remained pregnant than LPS or LPS + Dex ewes (p = 0.05). In summary, an inflammatory response was elicited by LPS and resulted in reduced pregnancy outcome, regardless of DEX administration. Treatment with TNF-alpha did not affect pregnancy outcome, possibly explained by low serum TNF-alpha levels. These data show that a sustained inflammatory response during early pregnancy leads to increased embryonic loss.