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Interleukin-18 involvement in hypoxic-ischemic brain injury
Maj Hedtjärn1, Anna-Lena Leverin, Kristina Eriksson
1Department of Physiology and Pharmacology, Perinatal Center, Göteborg University, 405 30 Göteborg, Sweden.
Summary
Interleukin-18 (IL-18) increases in the brain after hypoxic-ischemic injury. Blocking IL-18 reduces brain damage, indicating its role in hypoxic-ischemic brain injury development.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Inflammation significantly contributes to hypoxic-ischemic (HI) brain injury.
- Interleukin-18 (IL-18), a pro-inflammatory cytokine, is produced by microglia and activated by caspase-1.
Purpose of the Study:
- To characterize IL-18 and its receptor expression post-HI in relation to caspase-1 and IL-1beta.
- To evaluate the contribution of IL-18 to HI brain injury development.
Main Methods:
- Rats and mice underwent HI; brain tissue was analyzed for IL-18, caspase-1, and IL-1beta mRNA/protein expression.
- Immunohistochemistry assessed protein distribution.
- IL-18-deficient mice were compared to wild-type mice for brain injury severity.
Main Results:
- Caspase-1 and IL-18 expression increased post-HI, peaking later than IL-1beta.
- IL-18 and caspase-1 were found in microglia in the affected hemisphere.
- IL-18 deficiency significantly reduced infarct volume and neuropathology scores in multiple brain regions.
Conclusions:
- IL-18 expression in microglia is upregulated after HI.
- IL-18 plays a significant role in the pathogenesis of HI brain injury.