The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism.

@article{Fortier2004TheVM,
  title={The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism.},
  author={Marie-{\`E}ve Fortier and Stephen Kent and Helen F. Ashdown and Stephen Poole and Patricia Boksa and Giamal N. Luheshi},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2004},
  volume={287 4},
  pages={
          R759-66
        }
}
  • M. FortierS. Kent G. Luheshi
  • Published 1 October 2004
  • Biology
  • American journal of physiology. Regulatory, integrative and comparative physiology
Polyinosinic:polycytidylic acid (poly I:C) is a synthetic double-stranded RNA that is used experimentally to model viral infections in vivo. Previous studies investigating the inflammatory properties of this agent in rodents demonstrated that it is a potent pyrogen. However, the mechanisms underlying this response have not been fully elucidated. In the current study, we examined the effects of peripheral administration of poly I:C on body temperature and cytokine production. Male rats were… 
View on PubMed
ajpregu.physiology.org
295 Citations
Highly Influential Citations
23
Background Citations
111
Methods Citations
30
Results Citations
8

Figures from this paper

295 Citations

Fever and inflammatory cytokine response in rats injected subcutaneously with viral double-stranded RNA analog, polyinosinic:polycytidylic acid (Poly-I:C)

Central mediators involved in the febrile response induced by polyinosinic–polycytidylic acid: Lack of involvement of endothelins and substance P

Polyinosinic/Polycytidylic Acid–Mediated Changes in Maternal and Fetal Disposition of Lopinavir in Rats

The majority of commonly used and clinically important antiretroviral drugs are known to be ABC transporter substrates, and inflammation-mediated changes in transporter expression could affect their maternal disposition and fetal exposure.

The viral mimetic polyinosinic:polycytidylic acid (poly I:C) induces cellular responses in primary cultures from rat brain sites with an incomplete blood–brain barrier

Impact of Polyinosinic/Polycytidylic Acid on Placental and Hepatobiliary Drug Transporters in Pregnant Rats

The poly(I:C) model of viral infection imposes significant changes in the expression of key drug transporters in placental and hepatic tissues of pregnant rats.

The sickness behaviour and CNS inflammatory mediator profile induced by systemic challenge of mice with synthetic double-stranded RNA (poly I:C)

Synthetic double-stranded RNA polyinosinic-polycytidylic acid augments morphine-induced conditioned place preference in rats

The results show that the immune challenge by Poly I:C augmented morphine CPP in rats depending on the onset time of the challenge, and suggest that immune challenge may enhance the rewarding properties of opiates.

Expression patterns of innate immunity-related genes in response to polyinosinic:polycytidylic acid (poly[I:C]) stimulation in DF-1 chicken fibroblast cells

The results of this study may provide the basis for understanding host response to viral infection and its mimicry system in chickens.

Polyinosinic:polycytidylic acid induces memory processing deficits in the day-old chick

It is demonstrated that polyinosinic:polycytidylic acid induces memory processing deficits and is pyrogenic in the day-old chick and that these effects are cyclooxygenase-dependent.

Characterization of the febrile response induced by fibroblast-stimulating lipopeptide-1 in guinea pigs.

FSL-1-induced fever in guinea pigs depends, in shape and duration, on the route of administration and is, to a high degree, mediated by pyrogenic cytokines and COX products.
...

References

SHOWING 1-10 OF 49 REFERENCES

Dexamethasone pre-treatment is antipyretic toward polyinosinic: polycytidylic acid, lipopolysaccharide and interleukin 1/endogenous pyrogen

It is concluded that Poly I:C, LPS and IL1/E.P. induce fever by a common mechanism which is either directly or indirectly inhibited by dexamethasone.

The pyrogenic actions of the interferon-inducer, polyinosinic:polycytidylic acid are antagonised by ketoprofen.

Acute ethanol administration profoundly alters poly I:C-induced cytokine expression in mice by a mechanism that is not dependent on corticosterone.

Studies on poly I:C toxicity in experimental animals.

Polyriboinosinic:polyribocytidylic acid enhances rabbit slow-wave sleep.

It is concluded that poly I:C enhances slow-wave sleep and body temperature without provoking the acute-phase rise in plasma Cu, suggesting these effects may be initiated through an IFN-mediated process.

Prolonged effects of polyriboinosinic:polyribocytidylic acid on spontaneous running wheel activity and brain interferon-α mRNA in rats: a model for immunologically induced fatigue

Intratracheal double-stranded RNA plus interferon-gamma: a model for analysis of the acute phase response to respiratory viral infections.

Comparison of acute phase responses induced in rabbits by lipopolysaccharide and double-stranded RNA.

The primary distinctions between LPS and poly I:C with respect to cytokine induction in the RAW 264.7 macrophage cell line were that LPS failed to induce interferon (IFN)-alpha, poly I-C induced interleukin (IL)-6 mRNA minimally and for a shorter time period than did LPS, and LPS induced IL-1 alpha and IFN-beta more rapidly than did poly I;C.

Course of fever response to repeated administration of sublethal doses of lipopolysaccharides, polyinosinic: Polycytidylic acid and muramyl dipeptide to rabbits

It was observed that repeated injection of sublethal doses of LPS and MDP was connected with the changing of biphasic fever to monophasic, and the consequence of this was a drop in the fever index, while repeated administration of poly I:C did not result in such changes.

Polyinosinic acid: polycytidylic acid promotes T helper type 1‐specific immune responses by stimulating macrophage production of interferon‐α and interleukin‐12

The data suggest that poly I:C is a Th1‐inducing agent whose activity is mediated by its ability to stimulate the production of IFN‐α and IL‐12 by monocytes.