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Female Sex Hormones Influence the Febrile Response Induced by Lipopolysaccharide, Cytokines and Prostaglandins but not by Interleukin-1 beta in Rats
University of Federal Parana, Brazil.
University of Federal Parana, Brazil.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Akutkliniken.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
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2016 (Engelska)Ingår i: Journal of neuroendocrinology (Print), ISSN 0953-8194, E-ISSN 1365-2826, Vol. 28, nr 10Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

There are differences in the immune response, and particularly fever, between males and females. In the present study, we investigated how the febrile responses induced by lipopolysaccharide (LPS) and different endogenous pyrogens were affected by female gonadal hormones. The febrile response to i.p. injection of LPS (50g/kg) was 40% lower in female rats compared to male or ovariectomised (OVX) female rats. Accordingly, oestrogen replacement in OVX animals reduced LPS-induced fever. Treatment with the prostaglandin synthesis inhibitor indomethacin (2mg/kg, i.p. 30min before) reduced the febrile response induced by LPS in both OVX (88%) and sham-operated (71%) rats. In line with the enhanced fever in OVX rats, there was increased expression of cyclooxygenase-2 (COX-2) in the hypothalamus and elevated levels of prostaglandin E-2 (PGE(2)). In addition, OVX rats were hyper-responsive to PGE(2) injected i.c.v. By contrast to the enhanced fever in response to LPS and PGE(2), the febrile response induced by i.c.v. injection of interleukin (IL)-1 was unaffected by ovariectomy, whereas the responses induced by tumour necrosis factor (TNF)- and macrophage inflammatory protein (MIP)-1 were completely abrogated. These results suggest that the mediators involved in the febrile response in females are similar to males, although the reduction of female hormones may decrease the responsiveness of some mediators such as TNF- and MIP-1. Compensatory mechanisms may be activated in females after ovariectomy such as an augmented synthesis of COX-2 and PGE(2).

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell, 2016. Vol. 28, nr 10
Nyckelord [en]
fever, oestrogen, tumour necrosis factor-α, macrophage-inflammatory protein-1 beta
Nationell ämneskategori
Neurovetenskaper
Identifikatorer
URN: urn:nbn:se:liu:diva-132858DOI: 10.1111/jne.12414ISI: 000387066900003PubMedID: 27483048OAI: oai:DiVA.org:liu-132858DiVA, id: diva2:1052399
Anmärkning

Funding Agencies|Fundacao de Amparo a Pesquisa do Maranhao (FAPEMA) [00431/12]; Doctoral Abroad Program (PDSE)/CAPES, Brazil

Tillgänglig från: 2016-12-06 Skapad: 2016-11-30 Senast uppdaterad: 2018-01-13Bibliografiskt granskad

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Björk Wilhelms, Daniel

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Björk Wilhelms, DanielStojakovic, AndreaEngblom, David
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Avdelningen för cellbiologiMedicinska fakultetenAkutkliniken
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Journal of neuroendocrinology (Print)
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