Status epilepticus evokes prolonged increase in the expression of CCL3 and CCL4 mRNA and protein in the rat brain.

CCL3 and CCL4 are proinflammatory chemokines belonging to the CC family. Increase in expression of mRNA coding for various chemokines including CCL3 and CCL4 has been often detected with global transcriptome profiling of brain tissue following epileptogenic stimuli as well as in epilepsy in experimental models and in human patients. Despite this, little is known about the expression of these proteins in epileptogenesis or epilepsy. In the present work CCL3 and CCL4 mRNA and protein expression were studied in the amygdala stimulation model of temporal lobe epilepsy using quantitiative PCR and immunohistochemistry. Expression of CCL3 and CCL4 mRNA in the block of tissue containing enthorinal and piriform cortices, amygdala and piriform nucleus was markedly up-regulated at 1, 4, 14 and 30 days following stimulation and in hippocampal CA1 was significantly increased at 1 and 4 days following stimulation. Expression of CCL3 and CCL4 proteins was elevated in astrocytes in the enthorinal and piriform cortices, amygdala, and hippocampus showing the largest increase at 4D after status epilepticus. Increase in mRNA and protein levels of CCL3 and CCL4 in the animal model of temporal lobe epilepsy suggests their role in disease development or recovery form epileptogenic insult. Existence of multiple targets for these chemokines in the damaged brain allows several possibilities of influencing neuronal and glial functions.

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