Elevated levels of cerebrospinal fluid S100B are associated with brain injury and unfavorable outcomes in children with central nervous system infections

Peng, Qiongling; Tao, Shaohua; Nan, Yuemin; Peng, Yong-Zheng; Fu, Ning

doi:10.3109/00207454.2015.1135334

Cited by 23 publications

(15 citation statements)

References 36 publications

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“…Концентрация S100B достигала пика через 20 ч после заражения и оставалась высокой на протяжении всего эксперимента [22]. При БГМ у детей концентрация S100B коррелировала с тяжестью течения менингита и была независимым предиктором неблагоприятного исхода [24,25].…”

Section: новые методы диагностики бактериального менингитаunclassified

Diagnosis and current treatment of pneumococcal meningitis

Агаркова¹,

Покровский²,

Корокина³

et al. 2019

CPT

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Section: новые методы диагностики бактериального менингитаunclassified

Diagnosis and current treatment of pneumococcal meningitis

Агаркова¹,

Покровский²,

Корокина³

et al. 2019

CPT

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“…Further investigations, however, revealed that S100B in serum or CSF exhibited suboptimal sensitivity and specificity for bacterial meningitis. The highest, but still inconsistent, levels of S100B in CSF and serum were seen in viral encephalitis or in bacterial meningitis complicated by ventriculitis or obvious parenchymal abnormalities on brain imaging (44, 46). While many candidate cytokine and immunologic markers have shown promise as diagnostic tools in small studies, some have demonstrated conflicting findings across studies (Table 1).…”

Section: Cytokine-based Evaluation Of Csfmentioning

confidence: 99%

Neonatal Meningitis: Overcoming Challenges in Diagnosis, Prognosis, and Treatment with Omics

2017

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Neonatal meningitis is a devastating condition. Prognosis has not improved in decades, despite the advent of improved antimicrobial therapy and heightened index of suspicion among clinicians caring for affected infants. One in ten infants die from meningitis, and up to half of survivors develop significant lifelong complications, including seizures, impaired hearing and vision, and delayed or arrested development of such basic skills as talking and walking. At present, it is not possible to predict which infants will suffer poor outcomes. Early treatment is critical to promote more favorable outcomes, though diagnosis of meningitis in infants is technically challenging, time-intensive, and invasive. Profound neuronal injury has long been described in the setting of neonatal meningitis, as has elevated levels of many pro- and anti-inflammatory cytokines. Mechanisms of the host immune response that drive clearance of the offending organism and underlie brain injury due to meningitis are not well understood, however. In this review, we will discuss challenges in diagnosis, prognosis, and treatment of neonatal meningitis. We will highlight transcriptomic, proteomic, and metabolomic data that contribute to suggested mechanisms of inflammation and brain injury in this setting with a view toward fruitful areas for future investigation.

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“…It has been shown that enhancing peptides (EPs) derived from the co-receptor binding region of gp120 could promptly accelerated the formation of amyloid fibrils through the EP-derived nanofibers and significantly enhance HIV-1 infection3940. Recently, Zhang et al demonstrated that α7 nAChR plays a detrimental role in the host defense against CNS inflammation caused by microbial (e.g., meningitic pathogens and gp41) and non-microbial factors (e.g., METH) via the NF-κB signaling pathway12, which may be involved in regulation of the molecular marker (S100B) during various CNS disorders41. Similarly, the current study also showed that nicotine could upregulateα7 nAChR through activation of RAGE and S100B in the dentate gyrus (DG) of the hippocampus upon exposure to gp120, METH or NT in vivo , meanwhile the decrease of α7 nAChR and RAGE alleviated leukocyte (HL60 cell) transmigration across the HBMEC monolayers.…”

Section: Disscussionmentioning

confidence: 99%

Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine

Liu

et al. 2017

Sci Rep

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One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR). Both in vitro (human BMEC) (HBMEC) and in vivo (mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT. Aβ release from and transport across HBMEC were significantly increased by these factors. Methyllycaconitine (MLA), an antagonist of α7 nAChR, could efficiently block these pathogenic effects. Furthermore, our animal data showed that these factors could significantly increase the levels of Aβ, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1) in mouse cerebrospinal fluid (CSF) and Aβ in the mouse brains. These pathogenicities were significantly reduced by MLA, suggesting that α7 nAChR may play an important role in neuropathology caused by gp120, METH and NT, which are the major pathogenic factors contributing to the pathogenesis of HAND.

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Elevated levels of cerebrospinal fluid S100B are associated with brain injury and unfavorable outcomes in children with central nervous system infections

Abstract: This study has demonstrated that elevated levels of CSF S100B are associated with brain injury and could be used as an independent predictor of clinically unfavorable outcomes at discharge in children with CNS infections.

Cited by 23 publications

References 36 publications

Diagnosis and current treatment of pneumococcal meningitis

Diagnosis and current treatment of pneumococcal meningitis

Neonatal Meningitis: Overcoming Challenges in Diagnosis, Prognosis, and Treatment with Omics

Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine

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