Interleukin-1 as a Pathogenetic Mediator of Ischemic Brain Damage in Rats

Abstract

Application of rhIL-1 beta augmented the increase of brain water content, and application of anti-IL-1 beta depressed the increase of water content. These results tended to correlate with the neutrophilic infiltration into the parenchyma. It thus appears that IL-1 beta may play an important role in ischemic brain damage after reperfusion.

Interleukin-1β Inhibition Prevents Choroidal Neovascularization and Does Not Exacerbate Photoreceptor Degeneration

“…Previous reports have shown that IL-1␤ develops neurotoxic properties in the brain. 5,13,32 However, in the retina IL-1␤ was shown to inhibit ganglion cell death, 6 and IL-1␤ substitution saved photoreceptors in light-induced models 7 and genetic retinal degeneration. 8 Here, we show that IL-1␤ is significantly induced in the light-induced model in albino rats ( Figure 4D) and in albino mice ( Figure 5B).…”

“…1 IL-1␤ is a potent inflammatory mediator with chemotactic 2 and angiogenic 3,4 properties. It is a neurotoxic mediator in ischemic brain injury 5 but can attenuate glutamate neurotoxicity in the retina 6 and protect against light-induced or hereditary photoreceptor degeneration. 7,8 Age-related macular degeneration (AMD) is the leading cause of vision loss in elderly persons in industrialized countries.…”

Inhibition of interleukin 1β converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage

“…Furthermore, the appearance of cleavage products was decreased by z-VAD.FMK as was brain IL-1␤ levels 30 min after reperfusion. Treatments that reduce or antagonize the action of IL-1␤ (e.g., recombinant IL-1␤ antibodies or zinc protoporphyrin administration) decrease brain water content in ischemic brain (46).…”

Inflammation, plasticity and real-time imaging after cerebral ischemia

“…Barone et al [9] demonstrated that blocking endogenous TNF signiWcantly reduced infarct size in rats with the permanent or transient middle cerebral artery occlusion. A role for IL-1 in the pathogenesis of ischemic brain damage is supported by increased infarction resulting from intracerebroventricular injection of this cytokine in rat brain and conversely, neuroprotective eVects of interleukin-1 receptor antagonist [88,114,141]. In addition, short-term treatments with the antimicrobial/antiinXammatory agent minocycline alone or in combination conferred neuroprotection in experimental stroke [3,137,142,143].…”