Prospective research of human parechovirus and cytokines in cerebrospinal fluid of young children less than one year with sepsis-like illness: Comparison with enterovirus

Park, Su Eun; Song, Duyeal; Shin, Kyung‐Hwa; Nam, Sang Ook; Ko, Ara; Kong, Jai-Yul; Kim, Young Mi; Yeon, Gyu Min; Lee, Yun-Jin

doi:10.1016/j.jcv.2019.08.006

Cited by 16 publications

(18 citation statements)

References 24 publications

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“…In studies using only CSF samples, pro-inflammatory CSF cytokines (TNF-α, IL-1, and IL-6) and anti-inflammatory cytokines (IL-4 and IL-10) were significantly lower in PeV-A than in EV CNS infections [ 14 ]. Another study evaluating only CSF cytokines in infants showed that some cytokines (IL-1β, IL-5, IL-6, IL-12, and IL-17) were higher in EV infection, while some cytokines (IL-2, IL-4, IL-7, and IL-13) were detected in higher concentrations in PeV-A3 infection [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children

Sasidharan

Hassan

Harrison

et al. 2020

Open Forum Infectious Diseases

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Background Enterovirus (EV) and Parechovirus type A3 (PeV-A3) cause infections ranging from asymptomatic to life-threatening. Host immune responses in children, particularly innate responses to PeV-A3, remain largely unknown. The aim of this study was to determine aspects of the cytokine/chemokine responses to EV and PeV-A3 in cerebrospinal fluid (CSF) and plasma obtained from children with systemic/central nervous system infection. Methods A total of 74 salvaged CSF samples (27 with EV, 23 PeV-A3, and 24 neither EV nor PeV-A3) and 35 paired blood samples (10 EV, 14 PeV-A3, and 11 neither) were studied. Concentrations of cytokines and chemokines were measured using a customized 21-plex MILLIPLEX MAP® Human Cytokine/Chemokine Magnetic Bead Panel. Additionally, clinical characteristics data for all the patients were collected from Electronic Medical Records to evaluate the potential association between the immune response and presentations. Results We demonstrate that EV and PeV-A3 infections induce different cytokine/chemokine immune responses in children. EV induces more robust responses in CSF with significantly elevated levels of fractalkine, IFN-α2, IFN-γ, IL-1Rα, IL-4, IL-8, and TNF-α ; PeV-A3 induces less robust or absent responses in CSF but robust responses in plasma with significantly higher concentrations of IFN-α2, IL-15, IL-1Rα, IP-10, and MCP-1 . Conclusions High cytokine/chemokine concentrations in plasma of PeV-A3 patients compared to EV patients could explain higher/more prolonged fever in PeV-A3 patients, whereas relatively low cytokine/chemokine concentrations in PeV-A3 CSF might explain the absence of CSF pleocytosis.

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Section: Discussionmentioning

confidence: 99%

Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children

Sasidharan

Hassan

Harrison

et al. 2020

Open Forum Infectious Diseases

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“…In humans, there are several studies describing the cytokine levels in central nervous system (CNS) infections, such as meningitis and encephalitis [ 19 – 21 ]. However, to the best of our knowledge, there are no studies specifically analysing the neuroinflammatory response to systemic inflammatory conditions, i.e.…”

Section: Introductionmentioning

confidence: 99%

Systemic inflammation alters the neuroinflammatory response: a prospective clinical trial in traumatic brain injury

Lassarén

Lindblad

Frostell

et al. 2021

J Neuroinflammation

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Background Neuroinflammation following traumatic brain injury (TBI) has been shown to be associated with secondary injury development; however, how systemic inflammatory mediators affect this is not fully understood. The aim of this study was to see how systemic inflammation affects markers of neuroinflammation, if this inflammatory response had a temporal correlation between compartments and how different compartments differ in cytokine composition. Methods TBI patients recruited to a previous randomised controlled trial studying the effects of the drug anakinra (Kineret®), a human recombinant interleukin-1 receptor antagonist (rhIL1ra), were used (n = 10 treatment arm, n = 10 control arm). Cytokine concentrations were measured in arterial and jugular venous samples twice a day, as well as in microdialysis-extracted brain extracellular fluid (ECF) following pooling every 6 h. C-reactive protein level (CRP), white blood cell count (WBC), temperature and confirmed systemic clinical infection were used as systemic markers of inflammation. Principal component analyses, linear mixed-effect models, cross-correlations and multiple factor analyses were used. Results Jugular and arterial blood held similar cytokine information content, but brain-ECF was markedly different. No clear arterial to jugular gradient could be seen. No substantial delayed temporal associations between blood and brain compartments were detected. The development of a systemic clinical infection resulted in a significant decrease of IL1-ra, G-CSF, PDGF-ABBB, MIP-1b and RANTES (p < 0.05, respectively) in brain-ECF, even if adjusting for injury severity and demographic factors, while an increase in several cytokines could be seen in arterial blood. Conclusions Systemic inflammation, and infection in particular, alters cytokine levels with different patterns seen in brain and in blood. Cerebral inflammatory monitoring provides independent information from arterial and jugular samples, which both demonstrate similar information content. These findings could present potential new treatment options in severe TBI patients, but novel prospective trials are warranted to confirm these associations. Graphical abstract

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“…[4][5][6][7] Moreover, the host-immune response during CNS infection, measured by, for example, cytokines and chemokines, appears to differ between pathogens, most likely representing different pathogeneses. [8][9][10] In addition, the cytokine/chemokine profile in the CSF may be used to differentiate between viral or autoimmune encephalitis. 11,12 In order to increase the understanding of the utility of CSF cytokines and chemokines as biomarkers in childhood CNS infections, we examined whether the expression of these molecules varied by age.…”

Section: Introductionmentioning

confidence: 99%

Age-related changes in the inflammatory responses to viral infections in the central nervous system during childhood

2021

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BACKGROUND: The developmental stages and function of immune cells in the central nervous system during infancy and childhood are poorly understood. We analyzed whether cytokine and chemokine profiles in children and adolescents with viral central nervous system infections were different depending on age. METHODS: The acute phase cerebrospinal fluid of 80 children (mean age 98 months, range 1-206 months) were analyzed for protein levels of interleukin-1β (IL-1β),

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Prospective research of human parechovirus and cytokines in cerebrospinal fluid of young children less than one year with sepsis-like illness: Comparison with enterovirus

Cited by 16 publications

References 24 publications

Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children

Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children

Systemic inflammation alters the neuroinflammatory response: a prospective clinical trial in traumatic brain injury

Age-related changes in the inflammatory responses to viral infections in the central nervous system during childhood

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