Cerebrospinal fluid cytokines in COVID-19: a review and meta-analysis

Devlin, Lily; Gombolay, Grace

doi:10.1007/s00415-023-11928-3

Cited by 6 publications

(4 citation statements)

References 43 publications

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“…The lower level of TNF-α in the RNA CSF -positive group compared with the negative group hints at a less intense immune response in the CNS of Neuro-COVID patients than expected. [71][72][73] In scientific and medical terms, these results contribute to our understanding of the complex interplay between SARS-CoV-2 and the nervous system. The maintenance of BBB integrity in the RNA CSF -positive group may indicate a protective mechanism, but the heightened neuronal damage suggests a direct impact of the virus on the CNS.…”

Section: Discussionmentioning

confidence: 99%

Current clinical findings of acute neurological syndromes after SARS‐CoV‐2 infection

Wang,

Ren

et al. 2024

MedComm

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Neuro‐COVID, a condition marked by persistent symptoms post‐COVID‐19 infection, notably affects various organs, with a particular focus on the central nervous system (CNS). Despite scant evidence of SARS‐CoV‐2 invasion in the CNS, the increasing incidence of Neuro‐COVID cases indicates the onset of acute neurological symptoms early in infection. The Omicron variant, distinguished by heightened neurotropism, penetrates the CNS via the olfactory bulb. This direct invasion induces inflammation and neuronal damage, emphasizing the need for vigilance regarding potential neurological complications. Our multicenter study represents a groundbreaking revelation, documenting the definite presence of SARS‐CoV‐2 in the cerebrospinal fluid (CSF) of a significant proportion of Neuro‐COVID patients. Furthermore, notable differences emerged between RNA‐CSF‐positive and negative patients, encompassing aspects such as blood–brain barrier integrity, extent of neuronal damage, and the activation status of inflammation. Despite inherent limitations, this research provides pivotal insights into the intricate interplay between SARS‐CoV‐2 and the CNS, underscoring the necessity for ongoing research to fully comprehend the virus's enduring effects on the CNS. The findings underscore the urgency of continuous investigation Neuro‐COVID to unravel the complexities of this relationship, and pivotal in addressing the long‐term consequences of COVID‐19 on neurological health.

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Section: Discussionmentioning

confidence: 99%

Current clinical findings of acute neurological syndromes after SARS‐CoV‐2 infection

Wang,

Ren

et al. 2024

MedComm

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“…More likely, neuroinflammation is the result of the extreme high concentration of pro-inflammatory cytokines released by infected cells of the respiratory tract, reaching the brain via the bloodstream and causing impairment of the blood-brain barrier integrity with subsequent invasion of immune cells into the brain parenchyma (Gupta et al, 2020; Krasemann, Haferkamp, et al, 2022; Liu et al, 2020; Meinhardt et al, 2024; Monje & Iwasaki, 2022; Shabani, Liu, & Su, 2023). Among the cytokines are interleukin 2R, interleukin 6, interleukin 8, tumor necrosis factor (TNF, also known as TNF-alpha) and, interestingly, also the anti-inflammatory interleukin-10 (Devlin & Gombolay, 2023; Liu et al, 2020). Macrophages and lymphocytes penetrate the blood-brain barrier, activate microglial cells and astrocytes and finally determine neuroinflammation (Almutairi et al, 2021; Brown et al, 2023; Gonçalves de Andrade et al, 2021; Hernández-Parra et al, 2023; Iadecola et al, 2020; Tremblay et al, 2020; Vanderheiden & Klein, 2022).…”

Section: Discussionmentioning

confidence: 99%

Microgliosis, astrogliosis and loss of aquaporin-4 polarity in frontal cortex of COVID-19 patients

Beiersdorfer,

Rotermund,

Schulz

et al. 2024

Preprint

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The severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), causing human coronavirus disease 2019 (COVID-19), not only affects the respiratory tract, but also impacts other organs including the brain. A considerable number of COVID-19 patients develop neuropsychiatric symptoms that may linger for weeks and months and contribute to “long-COVID”. While the neurological symptoms of COVID-19 are well described, the cellular mechanisms of neurologic disorders attributed to the infection are still enigmatic. Here, we studied the effect of an infection with SARS-CoV-2 on the structure and expression of marker proteins of astrocytes and microglial cells in the frontal cortex of patients who died from COVID-19 in comparison to non-COVID-19 controls. Most of COVID-19 patients had microglial cells with retracted processes and rounded and enlarged cell bodies in both gray and white matter, as visualized by anti-Iba1 staining and confocal fluorescence microscopy. In addition, gray matter astrocytes in COVID-19 patients were frequently labeled by intense anti-GFAP staining, whereas in non-COVID-19 controls, most gray matter astrocytes expressed little GFAP. The most striking difference between astrocytes in COVID-19 patients and controls was found by anti-aquaporin-4 (AQP4) staining. In COVID-19 patients, a large number of gray matter astrocytes showed an increase in AQP4. In addition, AQP4 polarity was lost and AQP4 covered the entire cell, including the cell body and all cell processes, while in controls, AQP4 immunostaining was mainly detected in endfeet around blood vessels and did not visualize the cell body. In summary, our data suggest neuroinflammation upon SARS-CoV-2 infection including microgliosis and astrogliosis, including loss of AQP4 polarity.

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“…Interestingly, CSF IL-8 levels were found to be elevated in cases of coronavirus disease 2019 (COVID-19) [170,171]. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) can affect multiple organs, including the brain, leading to neuropsychiatric symptoms and cognitive impairments in patients with COVID-19 [172,173].…”

Section: Il-8 and Csfmentioning

confidence: 99%

IL-8 (CXCL8) Correlations with Psychoneuroimmunological Processes and Neuropsychiatric Conditions

Shkundin,

Halaris

2024

JPM

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Interleukin-8 (IL-8/CXCL8), an essential CXC chemokine, significantly influences psychoneuroimmunological processes and affects neurological and psychiatric health. It exerts a profound effect on immune cell activation and brain function, suggesting potential roles in both neuroprotection and neuroinflammation. IL-8 production is stimulated by several factors, including reactive oxygen species (ROS) known to promote inflammation and disease progression. Additionally, CXCL8 gene polymorphisms can alter IL-8 production, leading to potential differences in disease susceptibility, progression, and severity across populations. IL-8 levels vary among neuropsychiatric conditions, demonstrating sensitivity to psychosocial stressors and disease severity. IL-8 can be detected in blood circulation, cerebrospinal fluid (CSF), and urine, making it a promising candidate for a broad-spectrum biomarker. This review highlights the need for further research on the diverse effects of IL-8 and the associated implications for personalized medicine. A thorough understanding of its complex role could lead to the development of more effective and personalized treatment strategies for neuropsychiatric conditions.

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Cerebrospinal fluid cytokines in COVID-19: a review and meta-analysis

Cited by 6 publications

References 43 publications

Current clinical findings of acute neurological syndromes after SARS‐CoV‐2 infection

Current clinical findings of acute neurological syndromes after SARS‐CoV‐2 infection

Microgliosis, astrogliosis and loss of aquaporin-4 polarity in frontal cortex of COVID-19 patients

IL-8 (CXCL8) Correlations with Psychoneuroimmunological Processes and Neuropsychiatric Conditions

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