Production of chemokines in respiratory syncytial virus infection with central nervous system manifestations

Kawashima, Hisashi; Kashiwagi, Yasuyo; Ioi, Hiroaki; Morıchı, Shinichiro; Oana, Shingo; Yamanaka, Gaku; Takekuma, Kouji; Hoshika, Akinori; Sawai, Jun; Kato, Yuichi

doi:10.1007/s10156-012-0418-3

Cited by 38 publications

(59 citation statements)

References 21 publications

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“…However, we did observe a modest dampening of the IL-4 response in the brains of LPSexposed mice with lung SeV infection. Brain injury has been reported in a small subset of human infants with lung RSV infection (17), although whether antenatal inflammation is a contributory mechanism remains to be confirmed.…”

Section: Discussionmentioning

confidence: 99%

“…Paradoxically, clinical and experimental observations suggest that even preterm neonates can mount exaggerated inflammatory responses to infectious stimuli that could contribute to chronic morbidity or mortality (13)(14)(15)(16)(17). The mechanisms underlying this "hyper-inflammatory" phenotype are not well understood, although some evidence implicates impaired innate and adaptive immune interactions that disrupt homeostatic balance (7).…”

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confidence: 99%

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Maternal inflammation modulates infant immune response patterns to viral lung challenge in a murine model

et al. 2014

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Background: Chorioamnionitis, an inflammatory gestational disorder, commonly precedes preterm delivery. Preterm infants may be at particular risk for inflammation-related morbidity related to infection, although the pathogenic mechanisms are unclear. We hypothesized that maternal inflammation modulates immune programming to drive postnatal inflammatory processes. Methods: We used a novel combined murine model to treat late gestation dams with low-dose lipopolysaccharide (LPS) and to secondarily challenge exposed neonates or weanlings with Sendai virus (SeV) lung infection. Multiple organs were analyzed to characterize age-specific postnatal immune and inflammatory responses. results: Maternal LPS treatment enhanced innate immune populations in the lungs, livers, and/or spleens of exposed neonates or weanlings. Secondary lung SeV infection variably affected neutrophil, macrophage, and dendritic cell proportions in multiple organs of exposed pups. Neonatal lung infection induced brain interleukin (IL)-4 expression, although this response was muted in LPS-exposed pups. Adaptive immune cells, including lung, lymph node, and thymic lymphocytes and lung CD4 cells expressing FoxP3, interferon (IFN)-γ, or IL-17, were variably prominent in LPS-exposed pups. conclusion: Maternal inflammation modifies postnatal immunity and augments systemic inflammatory responses to viral lung infection in an age-specific manner. We speculate that inflammatory modulation of the developing immune system contributes to chronic morbidity and mortality in preterm infants. c horioamnionitis, an antenatal inflammatory disorder, is detected in the majority of placentas following extremely preterm delivery (1). The resultant fetal inflammation has been associated with postnatal development of chronic inflammatory disorders, including retinopathy of prematurity, periventricular leukomalacia, bronchopulmonary dysplasia, and necrotizing enterocolitis (2-4). However, the pathogenic role of chorioamnionitis in neonatal morbidity, particularly regarding

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Maternal inflammation modulates infant immune response patterns to viral lung challenge in a murine model

et al. 2014

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“…A CSF analysis obtained from hRSV infected children with neurological complications suggests that the encephalopathy can be induced by a cytokine storm-like disease [48 ]. Patients recruited in this study showed high levels of NO x in the CNS and were found to be positive for hRSV [48 ]. In addition, increased levels of IL-6, IL-8, MCP-1/CCL2 and MIP-1b/CCL4 in the CSF were detected in all patients (Figure 3).…”

Section: Current Opinion In Immunologymentioning

confidence: 78%

“…Such complications are associated with increased levels of pro-inflammatory cytokines as well as detection of genetic material and anti-hRSV antibodies in the CSF (Figure 3) [11]. A CSF analysis obtained from hRSV infected children with neurological complications suggests that the encephalopathy can be induced by a cytokine storm-like disease [48 ]. Patients recruited in this study showed high levels of NO x in the CNS and were found to be positive for hRSV [48 ].…”

Section: Current Opinion In Immunologymentioning

confidence: 90%

“…In addition, increased levels of IL-6, IL-8, MCP-1/CCL2 and MIP-1b/CCL4 in the CSF were detected in all patients (Figure 3). Also, IFN-g and TNF-a were found to be altered in the CSF in of hRSVinfected patients [48 ]. Likewise, it is thought that CCL2 and CCL4 contribute to the CNS damage through the recruitment of macrophages, as it has been described for bacterial meningitis [48 ].…”

Section: Current Opinion In Immunologymentioning

confidence: 94%

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Inflammatory damage on respiratory and nervous systems due to hRSV infection

Böhmwald¹,

Espinoza²,

Becerra³

et al. 2015

Current Opinion in Immunology

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TLR4 and nucleolin influence cell injury, apoptosis and inflammatory factor expression in respiratory syncytial virus‐infected N2a neuronal cells

Lü

et al. 2019

J of Cellular Biochemistry

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Respiratory syncytial virus (RSV) infection was recently reported to be associated with central nervous system (CNS) symptoms and neurological complications; however, related studies are very limited. Moreover, the molecular mechanism underlying RSV neuropathogenesis is still unclear. Our previous study revealed that toll‐like receptor 4 (TLR4) and nucleolin (C23) could be modulated and that they played a role during RSV infection in mouse neuronal‐2a (N2a) cells. In the present study, the effects of silencing of TLR4 and C23 on RSV propagation and N2a cellular responses were examined by using RNA interference technology. Four N2a cell treatment groups were established, namely, a normal control group, RSV control group, TLR4 siRNA + RSV group, and C23 siRNA + RSV group. Expression changes in NeuN protein and colocalization of C23 and TLR4 with RSV F protein were assessed using confocal microscopy. Changes in TLR4 and C23 mRNA expression, TLR4, C23, TLR3, TLR7, and p‐NF‐κB protein expression, and interleukin (IL)‐8, IL‐6, and tumor necrosis factor (TNF‐α) cytokine secretion was measured using quantitative real‐time reverse‐transcription polymerase chain reaction, Western blot analysis, and enzyme‐linked immunosorbent assay, respectively. RSV titers and the apoptotic status of N2a cells were monitored using plaque formation assays and flow cytometry, respectively. The results indicated that TLR4 and C23 gene knockdown decreased the amount of F protein in RSV‐infected N2a cells, inhibited RSV propagation, attenuated N2a neuronal injury, diminished cell apoptosis levels, downregulated TLR3 and TLR7 protein expression, and reduced inflammatory protein expression. Therefore, TLR4 and C23 knockdown influences cell injury, apoptosis and inflammatory protein expression in RSV‐infected N2a cells.

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Production of chemokines in respiratory syncytial virus infection with central nervous system manifestations

Cited by 38 publications

References 21 publications

Maternal inflammation modulates infant immune response patterns to viral lung challenge in a murine model

Maternal inflammation modulates infant immune response patterns to viral lung challenge in a murine model

Inflammatory damage on respiratory and nervous systems due to hRSV infection

TLR4 and nucleolin influence cell injury, apoptosis and inflammatory factor expression in respiratory syncytial virus‐infected N2a neuronal cells

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