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Abstract
Epilepsy is one of the most common neurology diseases. It is characterized by recurrent, spontaneous seizures and accompanied by various comorbidities which can significantly affect a person's life. Accumulating evidence indicates an essential pathophysiological role for neuroinflammation in epilepsy, which involves activation of microglia and astrocytes, recruitment of peripheral leukocytes into the central nervous system, and release of some inflammatory mediators, including pro-inflammatory factors and anti-inflammatory cytokines. There is complex crosstalk between the central nervous system and peripheral immune responses associated with the progression of epilepsy. This review provides an update of current knowledge about the contribution of this crosstalk associated with epilepsy. Additionally, how gut microbiota is involved in epilepsy and its possible influence on crosstalk is also discussed. Such recent advances in understanding suggest innovative methods for targeting the molecules correlated with the crosstalk and may provide a better prognosis for patients diagnosed with epilepsy.
Highlights
Epilepsy, one of the most common neurology diseases, affects nearly 65 million individuals worldwide [1]
Seizures may induce blood–brain barrier (BBB) leakage [7], which may contribute to crosstalk between resident and peripheral immune responses; resultant BBB dysfunction may provide a favorable microenvironment for communication between peripheral immune cells and central nervous system (CNS) resident immune cells, which may be involved in neurogenesis, synaptogenesis, neurotransmission, and angiogenesis after epilepsy or seizures [8,9,10,11,12]
This review has focused on the crosstalk between CNS immunity and peripheral immunity in epilepsy (Fig.1), an interaction that possibly provides intervention targets for epilepsy, in particular the specific immune-associated signaling molecules involved in the crosstalk to treat drug-resistant epilepsy
Summary
One of the most common neurology diseases, affects nearly 65 million individuals worldwide [1]. It has been suggested that neuroinflammatory signals play a significant role in the progression of epilepsy [5], which involves different conditions, such as release of inflammatory factors (involving pro-inflammatory cytokines and antiinflammatory factors), activation of microglia and astrocytes, as well as recruitment of peripheral leukocytes into the central nervous system (CNS) [2, 6]. Neuroinflammation accompanied by microglial activation and the infiltration of monocytes was detected in both animal models and patients with temporal lobe epilepsy (TLE) [21,22,23]. A recent study has demonstrated that preventing CCR2+ monocytes from penetrating the brain following status epilepticus (SE) contributed to neuroprotective outcomes, including lessened BBB opening, dampened inflammation, and enhanced functional recovery [41]. Endogenous astrocytic transforming growth factor (TGF)-β signaling inhibits CCL5 generation via the nuclear factor-κB (NF-κB) signaling pathway, reducing CCL5mediated recruitment of macrophages and T-cells to undamaged places within an infected brain [48]
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