Evidence that increases of mitochondrial immunoreactive IL-1β by HIV-1 gp120 implicatein situcleavage of pro-IL-1β in the neocortex of rat

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Abstract
Immunoelectron microscopy analysis of brain tissue sections and rat-specific sandwich ELISA allowed the localization of interleukin-1β (IL-1β) immunoreactivity in the mitochondria and cytosol of neocortical tissue preparations from the brain of naive, untreated, rats and rats receiving a single daily injection into one lateral cerebral ventricle (i.c.v.) of bovine serum albumin (BSA; 100 ng/day) for seven consecutive days. Interestingly, seven days i.c.v. treatment with the HIV-1 coat protein gp120 (100 ng/day) enhances IL-1β immunoreactivity in the cellular fractions studied. Elevation of mitochondrial immunoreactive IL-1β levels seems to originate from the conversion operated by the interleukin converting enzyme (ICE) of mitochondrial pro-IL-1β; in fact, IL-1β increases reported in the ELISA experiments were paralleled by a decrease of the mitochondrial pro-IL-1β 31-kDa band in conjunction with enhanced expression of the p20 component of activated ICE. In conclusion, the present results demonstrate that gp120-enhanced neocortical expression of IL-1β originates, at least in part, from in situ cleavage of mitochondrial pro-IL-1β and suggest that this, together with the central role of the mitochondrion in the expression of programmed cell death, may be important for apoptosis induced by the viral coat protein in the brain of rats.

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