Heme oxygenase-1 induction by cobalt protoporphyrin enhances fever and inhibits pyrogenic tolerance to lipopolysaccharide

Heme oxygenase-1 (HO-1) is an enzyme that catalyzes degradation of the heme and regulates its availability for newly synthetized hemeproteins such as cyclooxygenases, NO synthases and cytochrome P450. Moreover, HO-1 activity modulates synthesis of cytokines and prostaglandins. All of these factors a...

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Bibliographic Details
Published in:Journal of thermal biology 2014-10, Vol.45, p.69-74
Main Authors: Piotrowski, Jakub, Jedrzejewski, Tomasz, Kozak, Wieslaw
Format: Article
Language:English
Subjects:
Activation
Animals
Bacteria
Cobalt
Cytokines
Dinoprostone - blood
Enzymes
Fever
Fever - etiology
Fever - metabolism
Heme oxygenase
Heme Oxygenase-1 - blood
Interleukin-6
Interleukin-6 - blood
Lipopolysaccharide
Lipopolysaccharides - toxicity
Male
Prostaglandin E2
Prostaglandins
Protoporphyrins - pharmacology
Pyrogenic tolerance
Pyrogens - toxicity
Rats
Rats, Wistar
Tolerances
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Summary:Heme oxygenase-1 (HO-1) is an enzyme that catalyzes degradation of the heme and regulates its availability for newly synthetized hemeproteins such as cyclooxygenases, NO synthases and cytochrome P450. Moreover, HO-1 activity modulates synthesis of cytokines and prostaglandins. All of these factors are well-defined components of fever and pyrogenic tolerance mechanisms. We examine the effect of HO-1 induction and activation using cobalt protoporphyrin (CoPP) on changes in body temperature (Tb), plasma levels of interleukin-6 (IL-6), prostaglandin E2 (PGE2) and HO-1 protein in the course of these processes. Intraperitoneally (i.p.) pre-treatment of rats with CoPP (5mgkg−1) significantly accelerated and enhanced the early stage of lipopolysaccharide (LPS)-induced fever and shortened a post-fever recovery to normal temperature. Pre-treatment with CoPP significantly potentiated the increase in plasma IL-6, PGE2 and HO-1 levels measured 4h after the LPS administration. Furthermore, induction of HO-1 attenuated the development of pyrogenic tolerance to repeated injections of LPS. Based on these data we conclude that heme oxygenase-1 may act as a physiological regulator of the febrile response intensity to bacterial infections. •We examine the effect of HO-1 induction on fever and pyrogenic tolerance to LPS.•Induction of HO-1 accelerated and enhanced the early stage of LPS induced fever.•Induction of HO-1 attenuates the development of pyrogenic tolerance to LPS.•HO-1 acts as physiological regulator of the febrile response intensity to infections.
ISSN:0306-4565
1879-0992
DOI:10.1016/j.jtherbio.2014.08.002