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(American Journal of Pathology. 1998;153:1377-1381.)
© 1998 American Society for Investigative Pathology

Short Communications

Intracerebroventricular Injection of Anti-Fas Activates the Hypothalamus-Pituitary-Adrenal Axis and Induces Peripheral Interleukin-6 and Serum Amyloid A in Mice

Comparison with Other Ligands of the Tumor Necrosis Factor/NerveGrowth Factor Receptor Superfamily

Fabio Benigni* , Silvano Sacco* , Luigi Aloe{dagger} and Pietro Ghezzi*

From the Laboratory of Neuroimmunology,* Mario Negri Institute for Pharmacological Research, Milano, and the Institute of Neurobiology,{dagger} Consiglio Nazionale delle Ricerche, Rome, Italy

Fas is a receptor of the tumor necrosis factor (TNF)/nerve growth factor (NGF) receptor superfamily that mediates apoptosis and some inflammatory changes. As the central administration of TNF is known to activate the hypothalamus-pituitary-adrenal axis (HPAA) and to induce peripheral responses including induction of serum interleukin (IL)-6 and serum amyloid A (SAA), we investigated the effects of intracerebroventricular (i.c.v.) administration of agonist anti-Fas monoclonal antibody Jo2. Centrally administered anti-Fas (1 µg/mouse, i.c.v.) induced elevated levels of corticosterone, IL-6, and SAA comparable to those observed after i.c.v. administration of recombinant murine TNF. On the other hand, administration of murine NGF did not elevate serum corticosterone or IL-6, but induced SAA. Thus, Fas can trigger a centrally mediated anti-inflammatory response (HPAA activation) and induce a peripheral acute-phase response comparable to that induced with TNF, whereas NGF induces only acute-phase proteins.






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Copyright © 1998 by the American Society for Investigative Pathology.