Protein expression profiling of inflammatory mediators in human temporal lobe epilepsy reveals co-activation of multiple chemokines and cytokines

Kan, Anne A; de Jager, Wilco; de Wit, Marina; Heijnen, Cobi; van Zuiden, Mirjam; Ferrier, Cyrill; van Rijen, Peter; Gosselaar, Peter; Hessel, Ellen; van Nieuwenhuizen, Onno; de Graan, Pierre N E

doi:10.1186/1742-2094-9-207

Journal of Neuroinflammation

Table 6 Summary of potential pro-and anti-epileptogenic properties of inflammatory mediators

From: Protein expression profiling of inflammatory mediators in human temporal lobe epilepsy reveals co-activation of multiple chemokines and cytokines

“Pro-epileptogenic”			“Anti-epileptogenic”
*Protein*	*Function in CNS*	*reference*	*Protein*	*Function in CNS*	*reference*
CCL2	- contributes to immune-cell recruitment across the BBB	[49]	IL-1ra	- An anti-infllammatory protein with seizure inhibiting properties in experimental TLE	[50–53]
CCL3	- Capable of inducing Ca²⁺ transients in neuronal and microglial cultures.	[22, 54]	IL-7	Neurotrophic actions in embryonic brain cultures	[55, 56]
	- Inhibition of systemic receptor leads to decrease in seizure activity
CCL4	- Capable of inducing Ca²⁺ transients in neuronal and microglial cultures.	[22, 54]	IL-10	- Inhibits development of seizures in FS and a hypoxia model for epilepsy.	[57–60]
				- SNPs that result in increased IL-10 are decreased in FS patients.
	- Inhibition of systemic receptor leads to decrease in seizure activity
				-Can give trophic support to neurons
CCL5	- Capable of inducing Ca²⁺ transients in neuronal and microglial cultures	[22, 49, 54, 61]	IL-13	- Protects BBB integrity.	[62]
	- Glut release from CNS cells in hypothalamus
	- contributes to immune-cell recruitment across the BBB
	- Inhibition of systemic receptor leads to decrease in seizure activity
CCL19	immune-cell recruitment across the BBB.	[63, 64]	IL-25	- Protects BBB integrity	[62, 65]
CCL22	-Immune-cell recruitment across the BBB.	[66, 67]	IL-27	Marked anti-inflammatory actions in EAE.	[68, 69]
CXCL9	-Immune-cell recruitment across the BBB.	[70–72]	IFNα	- Suppression of hippocampal CA1 neurons & LTP	[73, 74]
IL-1α	Polymorphisms that lead to increased transcription are associated with TLE	[75–77]	HGF	- Enhances neuronal survival	[78, 79]
IL-1β	- Increased NMDA R subunit NR2B phosphorylation leading to increased Ca²⁺ influx	[80]^,[25, 52, 81, 82]	VEGF	- neuroprotective after experimental seizures	[83–85]
				- reduces hippocampal excitability
	- Higher levels correlate with increased SRS after eFS
IL-5	- Implicated in BBB disruption in CNS tumor bloodvessels	[86–88]	IL-5	- Anti-inflammatory actions in the periphery as a Th2 cytokine	[87–89]
	- Induces microglial proliferation
				- Induces microglial activation
IL-7	Induces neuronal apoptosis in human NT2 cells	[90]
IL-22	- BBB disruption through down-regulation of occludin.	[91]
VEGF	BBB disruption → reduction in tight junction proteins in kainate model for TLE	[92, 93].
ICAM-1	- implicated in BBB disruption	[20]
VCAM-1	- Immune-cell recruitment across the BBB	[20]

Abbreviations: BBB blood brain barrier, CNS central nervous system, SRS spontaneous recurrent seizure activity, NMDA N-methyl D-aspartate, NR2B N-methyl D-aspartate receptor subtype 2B, eFS experimental febrile seizures, NT2 neuronal teratocarcinoma Tera 2, FS febrile seizures, LTP long term potentiation, EAE experimental autoimmune encephalitis, SNP single nucleotide polymorphism.

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ISSN: 1742-2094

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