Elevated CSF IL-6 in a patient with respiratory syncytial virus encephalopathy

Otake, Yuko; Yamagata, Takanori; Morimoto, Yosuke; Imi, Mari; Mori, Masayuki; Aihara, Toshinori; Ichiyama, Takashi; Momoi, Mariko Y.

doi:10.1016/j.braindev.2006.06.008

Cited by 37 publications

(46 citation statements)

References 9 publications

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“…Recent studies have shown that cytokines and free radicals play important roles in acute encephalopathies [10]. In all types of acute encephalopathy, the production of excessive levels of inflammatory cytokines in systemic organs or the brain is suspected to induce mitochondrial and vascular endothelial disorders and apoptosis [11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Classification of acute encephalopathy in respiratory syncytial virus infection

Morıchı

Kawashima

Ioi

et al. 2011

Journal of Infection and Chemotherapy

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Section: Introductionmentioning

confidence: 99%

Classification of acute encephalopathy in respiratory syncytial virus infection

Morıchı

Kawashima

Ioi

et al. 2011

Journal of Infection and Chemotherapy

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“…Several reports have shown that increased proinflammatory cytokine levels, particularly IL-6, are correlated with the development of encephalopathy in various viral infections. [17][18][19][20][21] Influenza-associated encephalopathy is thought to be a consequence of systemic immune responses, 18,19 and high plasma concentrations of IL-6 can predict the development of influenza-associated encephalopathy. 18 Infants with encephalopathy associated with primary HHV-6 infection show higher serum and CSF levels of IL-6.…”

Section: Cns Dysfunctionmentioning

confidence: 99%

“…Increased proinflammatory cytokines are considered to play pathogenic roles in the development of CNS manifestations in various viral infections, including influenza virus, [17][18][19] respiratory syncytial virus infection 20 and primary HHV-6 infection. 21 SCT recipients are considered to have a tendency to display hypercytokinemia in the early phase of SCT because of engraftment syndrome (ES), 22 GVHD 23 or infectious diseases.…”

Section: Introductionmentioning

confidence: 99%

Correlations of HHV-6 viral load and plasma IL-6 concentration with HHV-6 encephalitis in allogeneic stem cell transplant recipients

Ogata

Satou

Kawano

et al. 2009

Bone Marrow Transplant

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This study investigated factors associated with the development of human herpesvirus (HHV)-6 encephalitis. Among 111 enrolled subjects, 12 patients developed central nervous system (CNS) dysfunction. CNS dysfunction in four patients was found to have no association with HHV-6. The remaining eight patients displayed HHV-6 encephalitis (n ¼ 3), limbic encephalitis (HHV-6 DNA in cerebrospinal fluid was not examined; n ¼ 3) or CNS dysfunction because of an unidentified cause (n ¼ 2). Realtime PCR showed CNS dysfunction in the latter eight patients, which developed concomitant with the appearance of high plasma levels of HHV-6 DNA (X10 4 copies/ml). Overall, eight of the 24 patients with high-level HHV-6 DNA developed CNS dysfunction, whereas no patients developed CNS dysfunction potentially associated with HHV-6 infection if peak HHV-6 DNA was o10 4 copies/ ml. We next analyzed plasma concentrations of IL-6, IL-10 and tumor necrosis factor-a among patients who displayed high-level plasma HHV-6 DNA and found elevated IL-6 concentrations preceding HHV-6 infection in patients who developed CNS dysfunction. (Mean ± s.d.: 865.7 ± 1036.3 pg/ml in patients with CNS dysfunction; 56.5±192.9 pg/ml in others; P ¼ 0.01). These results suggest that high-level HHV-6 load is necessary for the development of HHV-6 encephalitis, and systemic inflammatory conditions before HHV-6 infection form the preparatory conditions for progression to encephalopathy.

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“…Thus, an increased level of these proteins reflects the degree of damage to the BCB. On the other hand, small proteins such as IL-6 and IgG are produced in the intrathecal spaces as well as transported from the intravascular space [13,14]. Therefore, the content of these proteins reflects the degree of inflammation in the intrathecal space, but not the permeability of the BCB.…”

Section: Discussionmentioning

confidence: 98%