Glial cells and neurologic autoimmune disorders

Li, Zhao-Qing; Li, Tongxin; Tian, Ming; Ren, Ze-Sheng; Yuan, Chen-Yi; Yang, Rui-Kun; Shi, Su-Juan; Li, Hui; Kou, Zhenzhen

doi:10.3389/fncel.2022.1028653

Cited by 8 publications

(3 citation statements)

References 93 publications

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“…Autoimmune responses triggered by COVID-19 may also contribute to nervous system injury by targeting glial cells and blood vessels. Autoantibodies binding astrocytes and oligodendrocytes can disrupt the homeostasis and function of these glial cells, which support and interact with neurons (52). Anti-endothelial cell autoantibodies can promote apoptosis of vascular endothelial cells lining the blood-brain barrier, leading to microhemorrhages and facilitating neuroinflammation, and although this increase is uncommon in infected patients in the acute phase of COVID-19, it cannot be ruled out in long COVID (53).…”

Section: Glial Cell and Vascular Damage Induced By Autoimmunitymentioning

confidence: 99%

Neurological risks of COVID-19 in women: the complex immunology underpinning sex differences

Gu,

Zhang,

Liu

et al. 2023

Front. Immunol.

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The COVID-19 pandemic has uncovered many mysteries about SARS-CoV-2, including its potential to trigger abnormal autoimmune responses. Emerging evidence suggests women may face higher risks from COVID-induced autoimmunity manifesting as persistent neurological symptoms. Elucidating the mechanisms underlying this female susceptibility is now imperative. We synthesize key insights from existing studies on how COVID-19 infection can lead to immune tolerance loss, enabling autoreactive antibodies and lymphocyte production. These antibodies and lymphocytes infiltrate the central nervous system. Female sex hormones like estrogen and X-chromosome mediated effects likely contribute to dysregulated humoral immunity and cytokine profiles among women, increasing their predisposition. COVID-19 may also disrupt the delicate immunological balance of the female microbiome. These perturbations precipitate damage to neural damage through mechanisms like demyelination, neuroinflammation, and neurodegeneration – consistent with the observed neurological sequelae in women. An intentional focus on elucidating sex differences in COVID-19 pathogenesis is now needed to inform prognosis assessments and tailored interventions for female patients. From clinical monitoring to evaluating emerging immunomodulatory therapies, a nuanced women-centered approach considering the hormonal status and immunobiology will be vital to ensure equitable outcomes. Overall, deeper insights into the apparent female specificity of COVID-induced autoimmunity will accelerate the development of solutions mitigating associated neurological harm.

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Section: Glial Cell and Vascular Damage Induced By Autoimmunitymentioning

confidence: 99%

Neurological risks of COVID-19 in women: the complex immunology underpinning sex differences

Gu,

Zhang,

Liu

et al. 2023

Front. Immunol.

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“…The cause of such persistent neuroinflammation is not clear and may be effected by live residual bacteria impervious or inaccessible to antibiotics ( 12 , 13 ), anti- B. burgdorferi antibodies that cross react with nervous tissues, leading to glial activation ( 14 – 18 ), microbiome changes that affect the CNS through the gut-brain axis ( 19 , 20 ) and unresolved coinfections ( 21 ). In addition to these hypotheses, residual antigens after antibiotic treatment might also elicit (neuro)inflammation.…”

Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor receptor inhibitors mitigate the neuropathogenicity of Borrelia burgdorferi or its remnants ex vivo

Parthasarathy

2024

Front. Immunol.

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In previous studies, we showed that fibroblast growth factor receptors (FGFRs) contribute to inflammatory mediator output from primary rhesus microglia in response to live Borrelia burgdorferi. We also demonstrated that non-viable B. burgdorferi can be as pathogenic as live bacteria, if not more so, in both CNS and PNS tissues. In this study we assessed the effect of live and non-viable B. burgdorferi in inducing FGFR expression from rhesus frontal cortex (FC) and dorsal root ganglion (DRG) tissue explants as well as their neuronal/astrocyte localization. Specific FGFR inhibitors were also tested for their ability to attenuate inflammatory output and apoptosis in response to either live or non-viable organisms. Results show that in the FC, FGFR2 was the most abundantly expressed receptor followed by FGFR3 and FGFR1. Non-viable B. burgdorferi significantly upregulated FGFR3 more often than live bacteria, while the latter had a similar effect on FGFR1, although both treatments did affect the expressions of both receptors. FGFR2 was the least modulated in the FC tissues by the two treatments. FGFR1 expression was more prevalent in astrocytes while FGFR2 and FGFR3 showed higher expression in neurons. In the DRG, all three receptor expressions were also seen, but could not be distinguished from medium controls by immunofluorescence. Inhibition of FGFR1 by PD166866 downregulated both inflammation and apoptosis in both FC and DRG in response to either treatment in all the tissues tested. Inhibition of FGFR1-3 by AZD4547 similarly downregulated both inflammation and apoptosis in both FC and DRG in response to live bacteria, while with sonicated remnants, this effect was seen in one of the two FC tissues and 2 of 3 DRG tissues tested. CCL2 and IL-6 were the most downregulated mediators in the FC, while in the DRG it was CXCL8 and IL-6 in response to FGFR inhibition. Downregulation of at least two of these three mediators was observed to downregulate apoptosis levels in general. We show here that FGFR inhibition can be an effective anti-inflammatory treatment in antibiotic refractive neurological Lyme. Alternatively, two biologics may be needed to effectively curb neuroinflammation and pathology in the CNS and PNS.

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“…Glial cells, which play an important role in maintaining the stability and functional integrity of the central nervous system (CNS), constitute approximately half of all neural cells in the mammalian CNS [8]. Tere are mainly three types of glial cells in the CNS: microglia, astrocytes, and oligodendrocytes [9]. Over the past few decades, the function of diferent glial cells in physiological and pathological states has been explored deeply and widely.…”

Section: Introductionmentioning

confidence: 99%

Glial Cells of the Central Nervous System: A Potential Target in Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Lao,

Li,

Bai

et al. 2023

Pain Research and Management

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Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is one of the most common diseases of the male urological system while the etiology and treatment of CP/CPPS remain a thorny issue. Cumulative research suggested a potentially important role of glial cells in CP/CPPS. This narrative review retrospected literature and grasped the research process about glial cells and CP/CPPS. Three types of glial cells showed a crucial connection with general pain and psychosocial symptoms. Microglia might also be involved in lower urinary tract symptoms. Only microglia and astrocytes have been studied in the animal model of CP/CPPS. Activated microglia and reactive astrocytes were found to be involved in both pain and psychosocial symptoms of CP/CPPS. The possible mechanism might be to mediate the production of some inflammatory mediators and their interaction with neurons. Glial cells provide a new insight to understand the cause of complex symptoms of CP/CPPS and might become a novel target to develop new treatment options. However, the activation and action mechanism of glial cells in CP/CPPS needs to be further explored.

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Glial cells and neurologic autoimmune disorders

Cited by 8 publications

References 93 publications

Neurological risks of COVID-19 in women: the complex immunology underpinning sex differences

Neurological risks of COVID-19 in women: the complex immunology underpinning sex differences

Fibroblast growth factor receptor inhibitors mitigate the neuropathogenicity of Borrelia burgdorferi or its remnants ex vivo

Glial Cells of the Central Nervous System: A Potential Target in Chronic Prostatitis/Chronic Pelvic Pain Syndrome

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