Abstract
Bacterial meningitis (BM) is an acute infectious central nervous system (CNS) disease worldwide, occurring with 50% of the survivors left with a long-term serious sequela. Acute bacterial meningitis is more prevalent in resource-poor than resource-rich areas. The pathogenesis of BM involves complex mechanisms that are related to bacterial survival and multiplication in the bloodstream, increased permeability of blood–brain barrier (BBB), oxidative stress, and excessive inflammatory response in CNS. Considering drug-resistant bacteria increases the difficulty of meningitis treatment and the vaccine also has been limited to several serotypes, and the morbidity rate of BM still is very high. With recent development in neurology, there is promising progress for drug supplements of effectively preventing and treating BM. Several in vivo and in vitro studies have elaborated on understanding the significant mechanism of melatonin on BM. Melatonin is mainly secreted in the pineal gland and can cross the BBB. Melatonin and its metabolite have been reported as effective antioxidants and anti-inflammation, which are potentially useful as prevention and treatment therapy of BM. In bacterial meningitis, melatonin can play multiple protection effects in BM through various mechanisms, including immune response, antibacterial ability, the protection of BBB integrity, free radical scavenging, anti-inflammation, signaling pathways, and gut microbiome. This manuscript summarizes the major neuroprotective mechanisms of melatonin and explores the potential prevention and treatment approaches aimed at reducing morbidity and alleviating nerve injury of BM.
Highlights
Bacterial meningitis (BM) is the major cause of the central nervous system (CNS)infectious diseases among infants, adults, and older people, which usually induce high mortality and 50% of the survivors left permanent neurological sequelae [1,2]
The pathogenesis of BM mainly includes high-level bacteremia in the bloodstream, the destruction of the blood–brain barrier (BBB) integrity, and cerebrospinal fluid (CSF) pleocytosis, overwhelming inflammatory response in the CNS [3,5,6], which results in serious damage to the nervous system and even death
In hepatic ischemia/reperfusion study, mechanisms that melatonin effectively protect the liver by attenuating the increased level of MyD88, TLR3, and TLR4 protein expression have been intensively investigated, and it was been found that the inhibitory effects of melatonin on the MyD88 signaling pathway of TLR system was related with suppression of activation of NF-κ B, mitogen-activation protein kinase s (MAPKs), which contribute to the pathogenesis of bacterial meningitis processes [85,86,87]
Summary
Bacterial meningitis (BM) is the major cause of the central nervous system (CNS). infectious diseases among infants, adults, and older people, which usually induce high mortality and 50% of the survivors left permanent neurological sequelae [1,2]. The pathogenesis of BM mainly includes high-level bacteremia in the bloodstream, the destruction of the BBB integrity, and cerebrospinal fluid (CSF) pleocytosis, overwhelming inflammatory response in the CNS [3,5,6], which results in serious damage to the nervous system and even death. Melatonin with amphiphilicity can cross the BBB so that it enters the central nervous system (CNS) and the cerebrospinal fluid (CSF) [7] This is important for the effective prevention and treatment of CNS diseases after the supplement of exogenous melatonin. This review mainly focuses on the neuroprotective effects of melatonin, which include antibacterial, blocking the interaction of bacteria and receptors, protection of the BBB integrity, resisting oxidative stress, anti-inflammatory activity, and major signaling pathway in both in vivo and in vitro models
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