کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2442031 | 1108160 | 2005 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effect of Carprofen Treatment Following Experimentally Induced Escherichia coli Mastitis in Primiparous Cows
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کلمات کلیدی
complement component 5aNSAIDLBPPGE2primiparous cowTMBC5aCOXPIHsCD14TXB2tetramethylbenzidine - تترامتیل بنزیدینthromboxane B2 - ترومبوکسی B2nonsteroidal anti-inflammatory drug - داروهای ضد التهابی غیر استروئیدیRectal temperature - دما رکتومcyclo-oxygenase - سیکلو اکسیژنازHeart rate - ضربان قلبEscherichia coli mastitis - ماستیت اشرشیا کولیSoluble CD14 - محلول CD14LPS-binding protein - پروتئین اتصال دهنده LPSProstaglandin E2 - پروستاگلاندین E2Carprofen - کارپفن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
علوم دامی و جانورشناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Acute Escherichia coli mastitis is one of the major sources of economic loss in the dairy industry due to reduced milk production, treatment costs, discarded milk, and occasional fatal disease. Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used as adjunctive therapy to antibiotics. The objective of the current study was to evaluate the effect of carprofen treatment following infusion of Escherichia coli into the mammary glands of primiparous cows during the periparturient period. Severity of mastitis was scored based on the average milk production in the uninfected quarters on d +2 postinoculation and a clinical severity score. Carprofen was administered intravenously at 9Â h postchallenge, when clinical signs of mastitis appeared. In previous work, efficacy of NSAIDs was mainly evaluated using clinical symptoms. In the present study, the effect of carprofen on innate immune response was also assessed by quantification of inflammatory mediators. All primiparous cows reacted as moderate responders throughout the experimental period. Primiparous cows were intramammarily inoculated with 1Â ÃÂ 104 cfu of E. coli P4:O32 in 2 left quarters. Analysis of blood and milk parameters, including IL-8, complement component C5a, lipopolysaccharide-binding protein (LBP), soluble CD14, prostaglandin E2, and thromboxane B2 was performed from d 0 to d +6 relative to intramammary inoculation. Rectal temperature in carprofen-treated animals was lower than in control animals at 3 and 6Â h posttreatment. Treatment also restored the decreased reticulorumen motility that occurs during E. coli mastitis to preinfection levels faster than in control animals. Carprofen treatment resulted in an earlier normalization of the clinical severity score. Eicosanoid (prostaglandin E2 and thromboxane B2) production in milk tended to be inhibited by carprofen. No significant differences in the kinetic patterns of somatic cell count, IL-8, complement component C5a, LBP, and soluble CD14 were observed. In conclusion, carprofen treatment improved general clinical condition by effective antipyrexia and restoration of reticulorumen motility but did not significantly inhibit eicosanoid production. Carprofen treatment did not result in a significant decrease of chemotactic inflammatory mediators, IL-8 and C5a, and early innate immune molecules, sCD14 and LBP. Therefore, major modulatory effects from NSAID administration were not observed in this mastitis model, although a larger study might confirm some apparent trends obtained in the present results.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Dairy Science - Volume 88, Issue 7, July 2005, Pages 2361-2376
Journal: Journal of Dairy Science - Volume 88, Issue 7, July 2005, Pages 2361-2376
نویسندگان
F. Vangroenweghe, L. Duchateau, P. Boutet, P. Lekeux, P. Rainard, M.J. Paape, C. Burvenich,