Partial prostaglandin-mediated mechanism controlling the release of cortisol in plasma after intravenous administration of endotoxins

Massart-Leen, Am; Burvenich, Christian; Messom, G Vandeputte-Van; Hilderson, Hans

doi:10.1016/0739-7240(92)90015-p

Cited by 24 publications

(14 citation statements)

References 23 publications

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“…It has been well known that the HPA axis is activated in response to the treatment with LPS or cytokines; adrenal glucocorticoids, in turn, exert feedback effects on the immune system [5,9]. The pattern of endocrine responses as assessed by plasma profiles of ACTH and cortisol agreed with those reported previously in other breed of goats [7] and in sheep [3]. Plasma FFA elevation also tended to be biphasic while the increases of glucose was monophasic, but these changes were not significant statistically possibly due to relatively high concentrations of later samples in the vehicle treatment resulting perhaps from food deprivation during the experiment.…”

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confidence: 78%

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Pathophysiological Changes Evoked by Lipopolysaccharide Administration in Goats.

Takeuchi

Kikusui

Kizumi

et al. 1997

The Journal of Veterinary Medical Science

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ABSTRACT. To establish an adequate experimental model for the study of immuno-neuroendocrine mechanisms underlying the behavioral changes during the acute infection, temporal relationship of various physiological responses to endotoxin administration was examined in ovariectomized goats. Immediately after intravenous injection of 200 ng/kg of lipopolysaccharide, there were an abrupt decrease of white blood cell number and a gradual increase of rectal temperature, which were followed by elevation of plasma levels of adrenocorticotropic hormone, cortisol, glucose, free fatty acids, and then later by an increase of heart rate. The results suggest that the endotoxin administration would evoke a stereotyped cascade of, febrile, neuroendocrine and metabolic as well as autonomic response to the activation of immune systems in the ruminant species. -KEY WORDS: goat, HPA axis, lipopolysaccharide.J. Vet. Med. Sci. 59(2): 125-127, 1997 study in which the same dose generated acute behavioral responses such as reduction of feeding, rumination and grooming in ovariectomized goats [12]. One ml of vehicle (saline) or LPS solution (200 ng/kg) was injected at 10:00 via a jugular catheter. Each animal was treated repeatedly with vehicle and LPS, which were given on different days separated from each other by at least two weeks. Blood samples (1.5 ml) were collected at 20,

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confidence: 78%

“…Experimentally, the administration of lipopolysaccharide (LPS), an endotoxin of gram negative bacteria, has been shown to induce febrile responses, activate the hypothalamic-pituitary adrenal (HPA) axis, suppress gonadal and thyroid functions, and cause tachycardia in mammalian species [3,4,7,9,10,14].…”

mentioning

confidence: 99%

Pathophysiological Changes Evoked by Lipopolysaccharide Administration in Goats.

Takeuchi

Kikusui

Kizumi

et al. 1997

The Journal of Veterinary Medical Science

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“…The pro-inflammatory nature of LPS plays a critical role in the successful elimination of the infecting pathogen [75]. Furthermore, in many LPS-models the effect on several biological systems seems to be dependent on the dose [151]. Therefore, modulation rather than complete inhibition of the action of the LPS molecule is preferable.…”

Section: Modulation Of Severitymentioning

confidence: 99%

Severity of E. coli mastitis is mainly determined by cow factors

et al. 2003

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-Intramammary infections of dairy cows with Gram-positive bacteria such as Staphylococcus aureus (major cause of mastitis) have received a lot of attention because of their major economic impact on the dairy farm through production losses induced by an increase in somatic cell count. Management strategies, including greater awareness for efficient milking and hygienic measures, have limited the spread of Gram-positive bacteria and resulted in a significant decrease of proportion of S. aureus isolates and subclinical mastitis worldwide. Other organisms such as coliform subspecies and Streptococcus uberis, both environmental bacteria that cause clinical mastitis, have received less attention. Escherichia coli causes inflammation of the mammary gland in dairy cows around parturition and during early lactation with striking local and sometimes severe systemic clinical symptoms. This disease affects many high producing cows in dairy herds and may cause several cases of death per year in the most severe cases. It is well known that bacterial, cow and environmental factors are interdependent and influence mastitis susceptibility. Many studies, executed during the last decade, indicate that the severity of E. coli mastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. coli mastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, we know that the neutrophil is a key factor in the cows' defense against intramammary infection with E. coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infection and the outcome of E. coli mastitis. This review is a compilation of some major findings over the last 15 years concerning mainly host factors that modulate and influence neutrophil function and the mammary inflammatory reaction. The individual chapters address: virulence factors of E. coli strains, how neutrophils kill E. coli, connection between endotoxins, tumor necrosis factor-a and nitric oxide, severity classification of E. coli mastitis, lifespan of neutrophils, host factors that influence severity, tissue damage and production loss.

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“…Intravenous pretreatment with flurbiprofen abolished fever and delayed the changes in milk ion concentration (Burvenich et al, 1989). It has also been shown that the release of plasma cortisol after intravenous LPS administration is partially controlled by prostaglandins (Massart-Leën et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Effect of Carprofen Treatment Following Experimentally Induced Escherichia coli Mastitis in Primiparous Cows

Vangroenweghe

Duchateau

Boutet

et al. 2005

Journal of Dairy Science

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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 antiinflammatory 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 9 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 1 × 10 4 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 E 2 , and thromboxane B 2 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 6 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 2361in an earlier normalization of the clinical severity score. Eicosanoid (prostaglandin E 2 and thromboxane B 2 ) 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. (Key words: primiparous cow, carprofen, Escherichia coli mastitis, moderate inflammation) Abbreviation key: C5a = complement component 5a, COX = cyclo-oxygenase, HR = heart rate, LBP = LPSbinding protein, NSAID = nonsteroidal anti-inflammatory drug, PGE 2 = prostaglandin E 2 , PIH = postinfusion hour, RT = rectal temperature, sCD14 = soluble CD14, TMB = tetramethylbenzidine, TXB 2 = thromboxane B 2 .

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Partial prostaglandin-mediated mechanism controlling the release of cortisol in plasma after intravenous administration of endotoxins

Cited by 24 publications

References 23 publications

Pathophysiological Changes Evoked by Lipopolysaccharide Administration in Goats.

Pathophysiological Changes Evoked by Lipopolysaccharide Administration in Goats.

Severity of E. coli mastitis is mainly determined by cow factors

Effect of Carprofen Treatment Following Experimentally Induced Escherichia coli Mastitis in Primiparous Cows

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