15-keto-13-14-dihydroprostaglandin-f2alpha and Mastitis--Bovine

The aim of the study was to determine the effects of lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF), interleukin-1-alpha (IL-1α), and nitric oxide donor (NONOate) on both in vivo and in vitro secretion of prostaglandin (PG)E2, PGF2α, leukotriene (LT)B4, and LTC4 by the bovine mammary gland. In the first experiment, tissues isolated from the teat cavity and lactiferous sinus were treated in vitro with LPS (10 ng/mL), TNF (10 ng/mL), IL-1α (10 ng/mL), NONOate (10(-4) M), and the combination of TNF + IL-1α + NONOate for 4 or 8 h. PGE2 or PGF2α secretion was stimulated by all treatments (P < 0.05) excepting NONOate alone, which did not stimulate PGF2α secretion. Moreover, all factors increased LTB4 and LTC4 secretion (P < 0.05). In the second experiment, mastitis was experimentally mimicked in vivo by repeated (12 h apart) intramammary infusions (5 mL) of (1) sterile saline; (2) 250-μg LPS; (3) 1-μg/mL TNF; (4) 1-μg/mL IL-1α; (5) 12.8-μg/mL NONOate; and (6) TNF + IL-1α + NONOate into 2 udder quarters. All infused factors changed PGE2, 13,14-dihydro,15-keto-PGF2α, and LT concentrations in blood plasma collected from the caudal vena cava, the caudal superficial epigastric (milk) vein, the jugular vein, and the abdominal aorta (P < 0.05). In summary, LPS and other inflammatory mastitis mediators modulate PG and LT secretion by bovine mammary gland in both in vivo and in vitro studies.

Topics: Animals; Cattle; Cytokines; Dinoprost; Dinoprostone; Female; Interleukin-1alpha; Leukotriene B4; Leukotriene C4; Leukotrienes; Lipopolysaccharides; Mammary Glands, Animal; Mastitis, Bovine; Nitric Oxide; Nitric Oxide Donors; Prostaglandins; Tumor Necrosis Factor-alpha

Twenty-one, middle to late lactation Holstein cows were assigned to one of three treatments in a completely randomized design to examine physiological changes associated with intramammary or intravenous administration of Escherichia coli endotoxin. Treatments were 1) Hank's balanced salt solution infusion in two contralateral quarters (control), 2) E. coli endotoxin infusion in two contralateral quarters, and 3) intravenous infusion of E. coli endotoxin. Blood was sampled and rectal temperature was measured at 30-min intervals. Endotoxin treatment was at 0900 h and sampling continued until 1700 h. Serum prolactin, cortisol, and 13,14-dihydro-15-keto-prostaglandin F2 alpha were measured. A pyretic response was observed in intravenous and intramammary treatment groups after endotoxin treatment. Response peak was higher (41.1 vs. 40.3 degrees C) and occurred later (6 vs. 4.5 h posttreatment) in the intramammary than the intravenous treatment group. Significant prolactin peaks were observed also in intravenous and intramammary endotoxin treatment groups. Prolactin peaked higher (288 vs. 112 ng/ml) and occurred sooner (1 vs. 4 h posttreatment) in the intravenous than in the intramammary treatment group. Cortisol followed a trend similar to prolactin. Cortisol peaked higher (100 vs. 82 ng/ml) and sooner (2.5 vs. 4.5 h posttreatment) in the intravenous than in the intramammary treatment group. Concentrations of 13,14-dihydro-15-keto-prostaglandin F2 alpha increased rapidly posttreatment in the intravenous group only.

Topics: Abortion, Veterinary; Animals; Body Temperature; Cattle; Dinoprost; Endotoxins; Female; Hydrocortisone; Injections, Intravenous; Lactation; Mastitis, Bovine; Pregnancy; Prolactin; Random Allocation

Arachidonic acid metabolites (AAM) were measured in milk and plasma during the course of acute endotoxin-induced mastitis in 12 lactating cows. Mastitis was induced by intramammary challenge exposure with 10 micrograms of Escherichia coli (026:B6) endotoxin. Endotoxin was injected into the teat cistern via the teat canal of a single randomly selected rear quarter of each cow. Concentrations of prostaglandin (PG) F2 alpha and thromboxane (Tx) B2 in fat-free unextracted milk and of 15-keto-13,14-dihydro-PGF2 alpha in plasma were measured by radioimmunoassay. Total production of AAM in milk was determined by measuring quarter milk production. The AAM were compared in 6 cows administered flunixin meglumine (1.1 mg/kg of body weight) and in 6 cows administered saline solution. Concentrations of TxB2 in milk were significantly (P less than 0.001) increased during the early course of acute mastitis in endotoxin-treated quarters of cows not administered flunixin meglumine. Peak concentrations of TxB2 in milk occurred at 8 hours after endotoxin inoculation. Flunixin meglumine treatment produced significant (P less than 0.05) reductions in milk TxB2 and plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations. Concentrations of PGF2 alpha in milk and total PGF2 alpha and TxB2 production per quarter per milking were not significantly influenced by endotoxin challenge or by flunixin meglumine treatment.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Cattle; Clonixin; Dinoprost; Endotoxins; Escherichia coli; Female; Mastitis, Bovine; Milk; Nicotinic Acids; Prostaglandins F; Thromboxane B2