Thermoregulatory role of inducible nitric oxide synthase in lipopolysaccharide-induced hypothermia

Saia, Rafael Simone; Cárnio, Evelin Capellari

doi:10.1016/j.lfs.2006.04.010

Cited by 18 publications

(15 citation statements)

References 33 publications

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“…To test this possibility, daily rectal temperatures were measured in infected and uninfected mice. Measurement of febrile responses has been previously employed to follow disease after infection with various pathogens (5,36,39,42,44,47). Infected BALB/c mice showed no significant changes in their rectal temperatures after infection with C. burnetii NMII compared to uninfected mice.…”

Section: Resultsmentioning

confidence: 99%

“…One of the major immune responses against acute infections is fever, and febrile responses have been previously quantified as a parameter of disease after challenge of animals with different pathogens or in animals subjected to stress (5,36,39,42,44,47). Various bacterial components, including LPS, can stimulate a spectrum of host endogenous pyrogens to potentiate a fever response.…”

Section: Discussionmentioning

confidence: 99%

“…The measurement of febrile responses has been previously employed as a parameter to follow disease after challenge (5,36,39,42,44,47). Fever has been associated with improved survival during acute infections.…”

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confidence: 99%

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AttenuatedCoxiella burnetiiPhase II Causes a Febrile Response in Gamma Interferon Knockout and Toll-Like Receptor 2 Knockout Mice and Protects against Reinfection

et al. 2007

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Coxiella burnetii is a highly infectious obligate intracellular bacterium. The phase I form is responsible for Q fever, a febrile illness with flu-like symptoms that often goes undiagnosed. The attenuated C. burnetii phase II (having a truncated "O" chain of its lipopolysaccharide) does not cause disease in immunocompetent animals; however, phase II organisms remain infectious, and we questioned whether disease could be produced in immunodeficient mice. To study C.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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AttenuatedCoxiella burnetiiPhase II Causes a Febrile Response in Gamma Interferon Knockout and Toll-Like Receptor 2 Knockout Mice and Protects against Reinfection

et al. 2007

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“…However, the early hypothermia, which was observed in the present study and that has been reported to occur in response to LPS in rats (70,79), rabbits (88), and chicken (18), does not occur in mice (73). The early (starts within minutes) hypothermic response of rats occurring at LPS doses of 10 g/kg and higher clearly differs from the late (starts at 4 h or later) and prolonged (lasts 12 h or more) hypothermic response that develops in mice injected with extremely high (10,000 g/kg and higher) doses of LPS (38,73,75). Hence, mice cannot be used to study the early LPS hypothermia that is common for other species.…”

Section: Study Limitations and Design Considerationsmentioning

confidence: 99%

Cyclooxygenase-1 or -2—which one mediates lipopolysaccharide-induced hypothermia?

Steiner

Hunter²,

Phipps³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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DL, Romanovsky AA. Cyclooxygenase-1 or -2-which one mediates lipopolysaccharide-induced hypothermia? Am J Physiol Regul Integr Comp Physiol 297: R485-R494, 2009. First published June 10, 2009 doi:10.1152/ajpregu.91026.2008.-Systemic inflammation is associated with either fever or hypothermia. Fever, a response to mild systemic inflammation, is mediated by cyclooxygenase (COX)-2 and not by COX-1. However, it is still disputed whether COX-2, COX-1, neither, or both mediate(s) responses to severe systemic inflammation, and, in particular, the hypothermic response. We compared the effects of SC-236 (COX-2 inhibitor) and SC-560 (COX-1 inhibitor) on the deep body temperature (Tb) of rats injected with a lower (10 g/kg iv) or higher (1,000 g/kg iv) dose of LPS at different ambient temperatures (Tas). At a neutral Ta (30°C), the rats responded to LPS with a polyphasic fever (lower dose) or a brief hypothermia followed by fever (higher dose). SC-236 (2.5 mg/kg iv) blocked the fever induced by either LPS dose, whereas SC-560 (5 mg/kg iv) altered neither the febrile response to the lower LPS dose nor the fever component of the response to the higher dose. However, SC-560 blocked the initial hypothermia caused by the higher LPS dose. At a subneutral T a (22°C), the rats responded to LPS with early (70 -90 min, nadir) dose-dependent hypothermia. The hypothermic response to either dose was enhanced by SC-236 but blocked by SC-560. The hypothermic response to the higher LPS dose was associated with a fall in arterial blood pressure. This hypotensive response was attenuated by either SC-236 or SC-560. At the onset of LPS-induced hypothermia and hypotension, the functional activity of the COX-1 pathway (COX-1-mediated PGE2 synthesis ex vivo) increased in the spleen but not liver, lung, kidney, or brain. The expression of splenic COX-1 was unaffected by LPS. We conclude that COX-1, but not COX-2, mediates LPS hypothermia, and that both COX isoforms are required for LPS hypotension. body temperature; thermoregulation; fever; inflammation SO STRONGLY IS SYSTEMIC INFLAMMATION associated with changes in deep body temperature (T b ) that every clinical definition of the systemic inflammatory response syndrome includes a change in T b (11,48). Whereas the majority (ϳ90%) of patients with systemic inflammation have an increased T b , a number of them (ϳ10%) have a lowered T b (6, 17). Thermoregulatory manifestations are also present in animal models of systemic inflammation. In a rat model of systemic inflammation induced by bacterial LPS, the pattern of T b change depends on the ambient temperature (T a ) and the LPS dose. At a neutral or supraneutral T a (warm environment), fever is the prevailing response; the fever is monophasic when the dose of LPS is low (just suprathreshold), but it turns polyphasic as the dose increases (66, 68, 69, 71, 79); a mild hypothermia may precede the polyphasic fever when the dose of LPS is high (68). At a subneutral T a (cool environment), hypothermia followed by fever is the predominant response; th...

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“…Besides its role in hypovolemia and hypotension, overproduction of NO by inducible nitric oxide synthase has also been reported to play a role in lipopolysaccharide (LPS)-induced hypothermia, apparently through the regulation of AVP release [17] .…”

Section: Introductionmentioning

confidence: 99%

Thermoregulation and Vasopressin Secretion during Polymicrobial Sepsis

Oliveira-Pelegrin

Ravanelli²,

Branco³

et al. 2008

Neuroimmunomodulation

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Objective: We investigated the time course of thermoregulation, nitric oxide (NO) formation and hydroelectrolytic alterations, as well as mean arterial pressure and arginine vasopressin (AVP) secretion, in experimental sepsis induced by cecal ligation and puncture (CLP). Methods: Male Wistar rats submitted to CLP or a sham operation were divided into 4 groups, as follows: group 1, for survival rate evaluation for 24 h; group 2, for body temperature (Tb) analysis; group 3, for mean arterial pressure registration, and group 4, for blood collection and processing of the neurohypophysis and hypothalamic nuclei 0, 2, 4, 6 and 24 h after surgery. AVP levels and content were measured in plasma, neurohypophysis and the hypothalamic paraventricular and supraoptic nuclei. Results: Animals which underwent CLP showed high mortality, a progressive decrease in mean arterial pressure and an increase in plasma NO. Tb dropped during the first 4 h and showed a progressive increase 6 h after surgery. Plasma AVP levels increased immediately after CLP surgery and again at 6 h, before returning to basal levels at 24 h. This was followed by a depletion of neurohypophyseal AVP content at 4 h that continued until 24 h. AVP content in the supraoptic nucleus was elevated 24 h after CLP surgery, while in the paraventricular nucleus, an increase was observed at 6 h and 24 h. Conclusions: In the present study, laparotomy and hypotension may have been responsible for the increase in plasma AVP in the initial phase of polymicrobial sepsis, and this may have contributed to the observed hypothermia. Moreover, an apparently impaired replenishment of AVP content in the neurohypophysis, possibly due to increased NO formation, may explain the impaired AVP secretion in the late phase of severe sepsis.

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Thermoregulatory role of inducible nitric oxide synthase in lipopolysaccharide-induced hypothermia

Cited by 18 publications

References 33 publications

AttenuatedCoxiella burnetiiPhase II Causes a Febrile Response in Gamma Interferon Knockout and Toll-Like Receptor 2 Knockout Mice and Protects against Reinfection

AttenuatedCoxiella burnetiiPhase II Causes a Febrile Response in Gamma Interferon Knockout and Toll-Like Receptor 2 Knockout Mice and Protects against Reinfection

Cyclooxygenase-1 or -2—which one mediates lipopolysaccharide-induced hypothermia?

Thermoregulation and Vasopressin Secretion during Polymicrobial Sepsis

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