scholarly journals Immune-Induced Expression of Lipocalin-2 in Brain Endothelial Cells: Relationship with Interleukin-6, Cyclooxygenase-2 and the Febrile Response

2013 ◽  
Vol 25 (3) ◽  
pp. 271-280 ◽  
Author(s):  
N. Hamzic ◽  
A. Blomqvist ◽  
C. Nilsberth
Keyword(s):  
Endothelial Cells ◽  
Interleukin 6 ◽  
Cyclooxygenase 2 ◽  
Brain Endothelial Cells ◽  
Lipocalin 2 ◽  
Febrile Response ◽  
Induced Expression

scholarly journals Lipopolysaccharide-Induced Fever Depends on Prostaglandin E2 Production Specifically in Brain Endothelial Cells

Endocrinology ◽  
2012 ◽  
Vol 153 (10) ◽  
pp. 4849-4861 ◽  
Author(s):  
Linda Engström ◽  
Johan Ruud ◽  
Anna Eskilsson ◽  
Anders Larsson ◽  
Ludmila Mackerlova ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebrospinal Fluid ◽  
Prostaglandin E2 ◽  
Hematopoietic Cells ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Brain Endothelial Cells ◽  
Febrile Response ◽  
Pge2 Synthesis ◽  
The Brain

Abstract Immune-induced prostaglandin E2 (PGE2) synthesis is critical for fever and other centrally elicited disease symptoms. The production of PGE2 depends on cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (mPGES-1), but the identity of the cells involved has been a matter of controversy. We generated mice expressing mPGES-1 either in cells of hematopoietic or nonhematopoietic origin. Mice lacking mPGES-1 in hematopoietic cells displayed an intact febrile response to lipopolysaccharide, associated with elevated levels of PGE2 in the cerebrospinal fluid. In contrast, mice that expressed mPGES-1 only in hematopoietic cells, although displaying elevated PGE2 levels in plasma but not in the cerebrospinal fluid, showed no febrile response to lipopolysaccharide, thus pointing to the critical role of brain-derived PGE2 for fever. Immunohistochemical stainings showed that induced cyclooxygenase-2 expression in the brain exclusively occurred in endothelial cells, and quantitative PCR analysis on brain cells isolated by flow cytometry demonstrated that mPGES-1 is induced in endothelial cells and not in vascular wall macrophages. Similar analysis on liver cells showed induced expression in macrophages and not in endothelial cells, pointing at the distinct role for brain endothelial cells in PGE2 synthesis. These results identify the brain endothelial cells as the PGE2-producing cells critical for immune-induced fever.

Electron Microscopic Evidence for Induction of Cyclooxygenase-2 in Brain Endothelial Cells

1998 ◽  
Vol 856 (1 MOLECULAR MEC) ◽  
pp. 278-280 ◽  
Author(s):  
K. MATSUMURA ◽  
C. CAO ◽  
M. OZAKI ◽  
H. MORII ◽  
K. NAKADATE ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cyclooxygenase 2 ◽  
Brain Endothelial Cells ◽  
Electron Microscopic ◽  
Microscopic Evidence

Attenuated fever in pregnant rats is associated with blunted syntheses of brain cyclooxygenase-2 and PGE2

2002 ◽  
Vol 283 (6) ◽  
pp. R1346-R1353 ◽  
Author(s):  
Kyoko Imai-Matsumura ◽  
Kiyoshi Matsumura ◽  
Akira Terao ◽  
Yasuyoshi Watanabe
Keyword(s):  
Endothelial Cells ◽  
Cyclooxygenase 2 ◽  
Female Rats ◽  
Brain Endothelial Cells ◽  
Term Pregnancy ◽  
Pregnant Rats ◽  
Near Term ◽  
Fever Response ◽  
Colonic Temperature ◽  
The Brain

Attenuation of fever occurs in pregnant animals. This study examined a hypothesis that brain production of PGE2, the final mediator of fever, is suppressed in pregnant animals. Near-term pregnant rats and age-matched nonpregnant female rats were injected with lipopolysaccharide (100 μg/kg) intraperitoneally. Four hours later, colonic temperature was measured, their cerebrospinal fluid (CSF) was sampled for PGE2 assay, and their brains were processed for immunohistochemistry of cyclooxygenase-2, an enzyme involved in PGE2 biosynthesis. In the pregnant rats, lipopolysaccharide injection resulted in significantly smaller elevations in both colonic temperature and CSF-PGE2 level than in nonpregnant rats. In the pregnant rats, lipopolysaccharide-induced cyclooxygenase-2 expression was blunted in terms of the number of positive cells. There was a significant correlation between PGE2 level in CSF and the number of cyclooxygenase-2-positive endothelial cells. These results suggest that suppressed PGE2 production in the brain is one cause for the attenuated fever response at near-term pregnancy and that this suppressed PGE2 production is due to the suppressed induction of cyclooxygenase-2 in brain endothelial cells.

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