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Interferon- Potentiates Interleukin (IL)-6 and Tumor Necrosis Factor- But Not IL-1ß Induced by Endotoxin in the Brain

Istituto di Ricerche Farmacologiche Mario Negri, 20157 Milan, Italy

Address all correspondence and requests for reprints to: Dr. Maria Grazia De Simoni, Istituto Mario Negri, Via Eritrea 62, 20157 Milan, Italy. E-mail: de-simoni{at}irfmn.mnegri.it

Because interferon- (IFN) is present in the central nervous system during neurologic diseases associated with inflammation, its effect on endotoxin-induced cytokines was studied. Cerebrospinal fluid (CSF) and serum levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor- (TNF), their messenger RNA expression in brain areas (hypothalamus, hyppocampus, and striatum) and in spleen were evaluated 2 and 8 h after endotoxin [lipopolysaccharide (LPS), 25 µg/rat icv], IFN (2.5 µg/rat icv) or after their coadministration in rats. CSF and serum IL-1ß levels were increased by LPS alone and IFN coadministration did not furtherly increase them. IFN potentiated LPS effect on IL-6 and TNF levels in both CSF and serum. LPS and IFN- coadministration did not alter IL-1ß messenger RNA expression induced by LPS in brain areas and in spleen, but it potentiated that of IL-6 and TNF. The present in vivo data show that icv coadministration of LPS and IFN results in a potentiation of cytokine production (IL-6 and TNF) which may trigger a cascade of events relevant to neurodegenerative processes. This action is independent of IL-1ß because the production of this cytokine is not altered by IFN treatment.

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