SOME EFFECTS OF INTRAVENOUS PROSTAGLANDIN E<sub>1</sub> AND ENDOTOXIN IN YOUNG CHICKENS

Artunkal, Akgül A.; Marley, E.; Stephenson, John

doi:10.1111/j.1476-5381.1977.tb09736.x

Cited by 8 publications

(6 citation statements)

References 16 publications

(26 reference statements)

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“…Our first scenario is supported by evidence that 1) innate immune activation triggers the release of IL-6 in birds (9,27), 2) avian thrombocytes, a major component of the innate immune system in birds, upregulate their expression of IL-6 mRNA, as well as the important PG-synthesizing enzyme COX-2, after immune challenge (41), and 3) chickens develop fever following hypothalamic injection of PGE 2 (1). There is convincing evidence that IL-6 and PGE 2 are critically important for febrile mediation in mammals (5,29,35), even though the mechanism by which IL-6 instigates changes in the central nervous system to cause fever in mammals is still controversial.…”

Section: Effect Of Systemic Diclofenac On Centrally Induced Il-1␤ Fevermentioning

confidence: 76%

“…Although intracerebroventricular injection of PGE 1 and PGE 2 causes fever in chickens (1,2,30) and PG synthesis inhibitors have been shown to modulate the fever response in chickens and ducks (2,14,23), no one has demonstrated upregulated levels of PGs in the brain of febrile birds. In the present study, we abolished IL-1␤-induced fever with diclofenac, but we did not find PGE 2 to be upregulated in the CSF of febrile ducks, even though we measured PGE 2 concentrations at a time that coincided with T b values nearing the peak of the febrile response.…”

Section: Effect Of Systemic Diclofenac On Centrally Induced Il-1␤ Fevermentioning

confidence: 99%

“…With regard to PGs, intracerebroventricular injection of PGE 1 and PGE 2 induced fever in fowls and broilers (23,30,31) and young chicks (1,2) at thermoneutrality, but intracerebroventricular injection of PGF 2␣ and PGE 2 decreased the body temperature (T b ) of fowls and pigeons, respectively (31,32). The PG synthesis inhibitor indomethacin abolished LPS-induced fever in broilers (10 mg/kg iv) (23) but only reduced the duration of fever in young chicks (50 mg/kg iv) (2).…”

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confidence: 99%

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Brain IL-6- and PG-dependent actions of IL-1β and lipopolysaccharide in avian fever

Marais

Maloney

Gray

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Marais M, Maloney SK, Gray DA. Brain IL-6-and PG-dependent actions of IL-1␤ and lipopolysaccharide in avian fever. Am J Physiol Regul Integr Comp Physiol 301: R791-R800, 2011. First published June 15, 2011; doi:10.1152/ajpregu.00136.2011There is no persuasive evidence of a correlation between proinflammatory cytokines and avian fever. In this study, for the first time, we use avian cytokines to investigate a role for proinflammatory cytokines in the central component of avian fever. IL-1␤ and IL-6 injected intracerebroventricularly into Pekin ducks (n ϭ 8) initiated robust fevers of equal magnitude and duration, although there was a significant difference in the latency to a febrile response. In addition, the IL-1␤-induced fever could be abolished with an intracerebroventricular injection of antibodies to avian IL-6 or an oral administration of a PG synthesis inhibitor. Our findings indicate the following sequence of events within the central component of the avian febrile mechanism: IL-1␤ gives rise to bioactive IL-6, which stimulates an accelerated synthesis of PGs, and these PGs then adjust the sensitivity of warmsensitive neurons in the avian brain stem to mediate fever. Yet PGE 2 was not upregulated in the cerebrospinal fluid of ducks made febrile with LPS. We conclude that IL-1␤ and IL-6 may well mediate fever by instigating an accelerated synthesis of brain-derived PG, of a class other than PGE2, or that IL-6 serves as one of the terminal mediators of the avian febrile response.interleukin-1␤; interleukin-6; Pekin duck; prostaglandin E2 BIRDS, LIKE MAMMALS, DEVELOP fever when exposed to viruses and bacteria (25). The physiological mechanism responsible for febrile mediation in birds has not been elucidated. In homeothermic animals, thermoregulation is controlled by the central nervous system; therefore, fever, a nonthermal modifier of thermoregulation, requires adjustment of thermoregulatory controllers in the brain (35,46). The hypothalamus, with its temperature-sensitive neurons, serves as the dominant controller of temperature regulation in mammals, whereas the rostral brain stem is thought to house neurons that govern body temperature in birds (46). Despite these phylogenetic differences, it is clear that, in mammals and in birds, peripheral activation of the innate immune system results in physiological modifications at the site of thermoregulatory control.In mammals, proinflammatory cytokines, specifically IL-1␤ and IL-6, are known to act as mediators between the detection of an infectious stimulus by immune cells in the periphery and the stimulation of fever (5,(35)(36)(37). IL-1␤ is thought to activate IL-6, and circulating IL-6 concentrations are correlated with the upregulated expression of PG-synthesizing enzymes in the periphery and in brain vasculature (5,34,49). Humoral PGE 2 , produced by macrophages of the lungs and liver, was shown to initiate the first febrile phase in mammals (49), while subsequent febrile phases are thought to be mediated by an upregulated expression of PGE 2 in the br...

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Section: Effect Of Systemic Diclofenac On Centrally Induced Il-1␤ Fevermentioning

confidence: 76%

Section: Effect Of Systemic Diclofenac On Centrally Induced Il-1␤ Fevermentioning

confidence: 99%

mentioning

confidence: 99%

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Brain IL-6- and PG-dependent actions of IL-1β and lipopolysaccharide in avian fever

Marais

Maloney

Gray

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…All other studies available on avian fever report a monophasic fever regardless of whether LPS was I.V. injected [5,6,11,14] or intraperitoneally injected [15] into the hypothalamus [18] or I.C.V. [1,2].…”

Section: Discussionmentioning

confidence: 98%

“…Artunkal et al found in chicken that intrahypothalamic or I.V. injections of PGE 1 or PGE 2 induced hyperthermia in warm ambient temperature, but hypothermia in cold ambient temperature [14,18]. On the other hand, a dose-dependent hypothermic effect following I.C.V.…”

Section: Discussionmentioning

confidence: 99%

Role of Prostaglandin E2 and Indomethacin in the Febrile Response of Pigeons

Nomoto

2003

JJP

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Birds, like mammals, develop a febrile response after an injection of bacterial endotoxin [1][2][3][4][5][6][7][8][9] or following bacterial infection [10,11]. In most mammals, prostaglandin E 2 (PGE 2 ) has been found to be an important mediator of fever [12,13], though some studies of avian fever concluded that the central mechanism causing the febrile rise of core temperature (T core ) in birds differs from that in mammals. Although it has been described that the inhibitors of prostaglandin synthesis such as INDO or aspirin lower the febrile response in chickens [1,5] and pigeons [10], these findings cannot be generalized. Artunkal et al. found that the pyretic effect of intrahypothalamic injections of PGE 1 in chickens was intensified and prolonged after a blockade of prostaglandin synthesis with INDO [14]. Recently, Fraifeld et al. reported that systemic injection LPS elicited fever in chicken, but without an elevation of hypothalamic PGE 2 production [15]. Because of these conflicting results, the aim of the present study was to investigate the role of PGE 2 and INDO in fever generation in pigeons. MATERIALS AND METHODSThis study was approved by the Committee of Animal Care of Tokyo Metropolitan Institute of Gerontology. Twenty-four domestic pigeons (Columba livia) weighing 474.6Ϯ44.3 g (meanϮSD) were used in this study. Japanese Journal of Physiology, 53, 253-258, 2003 Key words: lipopolysaccharide, fever, indomethacin, prostaglandin E 2 , pigeon.Abstract: Intravenous (I.V.) injection of 10 g/ kg Escherichia coli lipopolysaccharide (LPS), applied at 13:00, evoked in pigeons a biphasic rise of core temperature (T core ), so that LPS induced with a latency of 30 min first a decrease of T core , and 90 min after LPS, T core increased, obtaining maximum values from 18:00 to 20:00.Prostaglandins have been considered to be importantly involved in fevers in mammals. To investigate an involvement of prostaglandins in the cyclic variations of T core in birds, pigeons were injected I.V. with either 10 mg/kg indomethacin (INDO) or 100 mg/kg aspirin, or they were treated with intracerebroventricular (I.C.V.) injections of 100 g/kg INDO at various times before or after LPS. When INDO or aspirin was I.V. injected 30 or 15 min before LPS, it diminished the initial decrease of T core by more than 50%, whereas the I.V. injection of these drugs 2 and 4 h after LPS did not affect the febrile rise of T core . I.C.V. injections of INDO given either before or after LPS neither influenced the initial drop of T core nor the following febrile hyperthermia. Both the I.V. injection of 1 mg/kg prostaglandin E 2 (PGE 2 ) and the I.C.V. injection of 1 g/kg PGE 2 lowered T core . Our observations suggest that prostaglandins are not involved in the febrile elevation of T core in pigeons, but appear to participate in the decrease of T core , which shortly follows the I.V. injection of LPS. This initial drop of T core following LPS may be caused by a peripheral action of prostaglandins because it was not influenced by the I.C.V. inje...

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Changes in body temperature after administration of acetylcholine, histamine, morphine, prostaglandins and related agents

Clark

1980

Neuroscience & Biobehavioral Reviews

137

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SOME EFFECTS OF INTRAVENOUS PROSTAGLANDIN E₁ AND ENDOTOXIN IN YOUNG CHICKENS

Cited by 8 publications

References 16 publications

Brain IL-6- and PG-dependent actions of IL-1β and lipopolysaccharide in avian fever

Brain IL-6- and PG-dependent actions of IL-1β and lipopolysaccharide in avian fever

Role of Prostaglandin E2 and Indomethacin in the Febrile Response of Pigeons

Changes in body temperature after administration of acetylcholine, histamine, morphine, prostaglandins and related agents

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SOME EFFECTS OF INTRAVENOUS PROSTAGLANDIN E1 AND ENDOTOXIN IN YOUNG CHICKENS

Cited by 8 publications

References 16 publications

Brain IL-6- and PG-dependent actions of IL-1β and lipopolysaccharide in avian fever

Brain IL-6- and PG-dependent actions of IL-1β and lipopolysaccharide in avian fever

Role of Prostaglandin E2 and Indomethacin in the Febrile Response of Pigeons

Changes in body temperature after administration of acetylcholine, histamine, morphine, prostaglandins and related agents

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Product

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SOME EFFECTS OF INTRAVENOUS PROSTAGLANDIN E₁ AND ENDOTOXIN IN YOUNG CHICKENS