Changes of CXCL12, CXCL14 and PDGF levels in the brain of patients with idiopathic demyelinating optic neuritis and neuromyelitis optica

Chen, Tingjun; Li, Zhaohui; Jiang, Zhaocai; Liu, Zihao; Xu, Quangang; Huang, Dehui; Lin, Qing; Wei, Shihui

doi:10.1016/j.jneuroim.2014.12.004

Cited by 10 publications

(6 citation statements)

References 56 publications

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“…CD14 + CD16 + monocytes transmigrate preferentially across the BBB in response to CXCL12 compared with CD14 + CD16 2 monocytes or T cells CXCL12 is expressed constitutively in the CNS and is increased in the brains of HIV-infected individuals with CNS pathology [29,30,[48][49][50]. We [8,23] and others [13,24,51] showed that CD14 + CD16 + monocytes are significantly increased in the peripheral blood of HIV-infected individuals and that these cells are key mediators of HIV CNS pathogenesis.…”

Section: Resultsmentioning

confidence: 99%

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Frontline Science: CXCR7 mediates CD14+CD16+ monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS

Veenstra

Williams

Calderon

et al. 2017

Journal of Leukocyte Biology

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CD14CD16 monocytes transmigrate into the CNS of HIV-positive people in response to chemokines elevated in the brains of infected individuals, including CXCL12. Entry of these cells leads to viral reservoirs, neuroinflammation, and neuronal damage. These may eventually lead to HIV-associated neurocognitive disorders. Although antiretroviral therapy (ART) has significantly improved the lives of HIV-infected people, the prevalence of cognitive deficits remains unchanged despite ART, still affecting >50% of infected individuals. There are no therapies to reduce these deficits or to prevent CNS entry of CD14CD16 monocytes. The goal of this study was to determine whether CXCR7, a receptor for CXCL12, is expressed on CD14CD16 monocytes and whether a small molecule CXCR7 antagonist (CCX771) can prevent CD14CD16 monocyte transmigration into the CNS. We showed for the first time that CXCR7 is on CD14CD16 monocytes and that it may be a therapeutic target to reduce their entry into the brain. We demonstrated that CD14CD16 monocytes and not the more abundant CD14CD16 monocytes or T cells transmigrate to low homeostatic levels of CXCL12. This may be a result of increased CXCR7 on CD14CD16 monocytes. We showed that CCX771 reduced transmigration of CD14CD16 monocytes but not of CD14CD16 monocytes from uninfected and HIV-infected individuals and that it reduced CXCL12-mediated chemotaxis of CD14CD16 monocytes. We propose that CXCR7 is a therapeutic target on CD14CD16 monocytes to limit their CNS entry, thereby reducing neuroinflammation, neuronal damage, and HIV-associated neurocognitive disorders. Our data also suggest that CCX771 may reduce CD14CD16 monocyte-mediated inflammation in other disorders.

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Section: Resultsmentioning

confidence: 99%

“…suggest that CD14 + CD16 + monocytes would transmigrate in response to the low levels of CXCL12 that are present during basal homeostatic conditions in the CNS [49,50], which may contribute to early infection of the CNS.…”

Section: Resultsmentioning

confidence: 99%

Frontline Science: CXCR7 mediates CD14+CD16+ monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS

Veenstra

Williams

Calderon

et al. 2017

Journal of Leukocyte Biology

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“…The procedure of AQP4 antibody detection in living cells was described previously 18. In terms of MOG antibodies testing, live HEK-293 cells were transiently transfected with a plasmid containing full-length human MOG cDNA before it exposed to the patients’ diluted serum.…”

Section: Methodsmentioning

confidence: 99%

Clinical features of demyelinating optic neuritis with seropositive myelin oligodendrocyte glycoprotein antibody in Chinese patients

et al. 2018

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“…Other protein factors with altered expression in LPFC layer 1 in autism include chemokine ligand 14 (CXCL14) and neuron-derived neurotrophic factor (NDNF). CXCL14, an inflammatory cytokine, is involved in the regulation of myelination; reduction in the expression of this cytokine results in a reduction in myelination [4, 119], which is consistent with our findings of reduced myelination and increased branching in prefrontal cortices of adults with autism [129, 131, 133]. NDNF is mainly expressed by Cajal-Retzius cells of layer 1, and promotes the growth and development of neuronal cell bodies and neurite outgrowth [70, 106].…”

Section: Discussionmentioning

confidence: 99%

Postnatal development and maturation of layer 1 in the lateral prefrontal cortex and its disruption in autism

Trutzer

García‐Cabezas

Zikopoulos

2019

acta neuropathol commun

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Autism is a neurodevelopmental connectivity disorder characterized by cortical network disorganization and imbalance in excitation/inhibition. However, little is known about the development of autism pathology and the disruption of laminar-specific excitatory and inhibitory cortical circuits. To begin to address these issues, we examined layer 1 of the lateral prefrontal cortex (LPFC), an area with prolonged development and maturation that is affected in autism. We focused on layer 1 because it contains a distinctive, diverse population of interneurons and glia, receives input from feedback and neuromodulatory pathways, and plays a critical role in the development, maturation, and function of the cortex. We used unbiased quantitative methods at high resolution to study the morphology, neurochemistry, distribution, and density of neurons and myelinated axons in post-mortem brain tissue from children and adults with and without autism. We cross-validated our findings through comparisons with neighboring anterior cingulate cortices and optimally-fixed non-human primate tissue. In neurotypical controls we found an increase in the density of myelinated axons from childhood to adulthood. Neuron density overall declined with age, paralleled by decreased density of inhibitory interneurons labeled by calretinin (CR), calbindin (CB), and parvalbumin (PV). Importantly, we found PV neurons in layer 1 of typically developing children, previously detected only perinatally. In autism there was disorganization of cortical networks within layer 1: children with autism had increased variability in the trajectories and thickness of myelinated axons in layer 1, while adults with autism had a reduction in the relative proportion of thin axons. Neurotypical postnatal changes in layer 1 of LPFC likely underlie refinement of cortical activity during maturation of cortical networks involved in cognition. Our findings suggest that disruption of the maturation of feedback pathways, rather than interneurons in layer 1, has a key role in the development of imbalance between excitation and inhibition in autism.

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Changes of CXCL12, CXCL14 and PDGF levels in the brain of patients with idiopathic demyelinating optic neuritis and neuromyelitis optica

Cited by 10 publications

References 56 publications

Frontline Science: CXCR7 mediates CD14+CD16+ monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS

Frontline Science: CXCR7 mediates CD14+CD16+ monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS

Clinical features of demyelinating optic neuritis with seropositive myelin oligodendrocyte glycoprotein antibody in Chinese patients

Postnatal development and maturation of layer 1 in the lateral prefrontal cortex and its disruption in autism

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