INCREASED INTERLEUKIN-6 PRODUCTION BY CEREBRAL CORTICAL TISSUE OF ADULT VERSUS YOUNG MICE

Citation
Mm. Prechel et al., INCREASED INTERLEUKIN-6 PRODUCTION BY CEREBRAL CORTICAL TISSUE OF ADULT VERSUS YOUNG MICE, Mechanism of ageing and development, 92(2-3), 1996, pp. 185-194
Citations number
33
Categorie Soggetti
Geiatric & Gerontology",Biology,"Cell Biology
ISSN journal
00476374
Volume
92
Issue
2-3
Year of publication
1996
Pages
185 - 194
Database
ISI
SICI code
0047-6374(1996)92:2-3<185:IIPBCC>2.0.ZU;2-X
Abstract
The cytokine interleukin-6 (IL-6) has been implicated as a contributor to injury in several neurological disorders. The amounts of IL-6 rele ased by the cerebral cortical tissue of mice of varying maturational a ge groups were measured and found to increase with age. Specifically, the basal level of IL-6 released from the tissue of infant (less than 2 weeks old) mice was low, although the tissue could be readily stimul ated to secrete high levels of IL-6. Higher levels of IL-6 were releas ed from young adult (2 month old) mice. Adult mice that were either 6 or 9 months of age secreted significantly higher levels of IL-6 compar ed to the tissue of either the young adult or infant animals, although the difference between levels secreted by the 6- or 9-month old group s was minimal. IL-6 production by adult cerebral cortical tissue could be further stimulated, but it was less readily achieved compared to t he tissue of infants. In response to the negative regulator transformi ng growth factor-beta (TGF-beta), the levels of IL-6 released by stimu lated cerebral cortical tissue of infants, as well as by unstimulated and stimulated tissue of adults, were reduced to the low basal levels of IL-6 produced by infant tissue. These results suggest that normal d evelopment and aging are correlated with an increase in IL-6 productio n that may be due to shifts in levels of stimulatory or inhibitory reg ulatory controls, but not to an inability of young tissue to produce I L-6 or to a lack of responsiveness of adult tissues to negative regula tory control by TGF-beta. (C) 1996 Elsevier Science Ireland Ltd.