Expression of Cytokines on Human Bronchial Epithelial Cells Induced by Influenza Virus A

Adachi, Mitsuru; Matsukura, Satoshi; Tokunaga, Hisahiro; Kokubu, Fumio

doi:10.1159/000237584

Cited by 76 publications

(52 citation statements)

References 4 publications

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“…Our model does not preclude a role for other stimuli besides endothelial infection to induce platelet-endothelial adhesion. For instance, influenza infection recently has been reported to induce lung epithelial cytokine production, including that of interleukin-6 (IL-6), IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF) (44,45,46). Similarly, activated neutrophils and macrophages which are recruited to the lung after influenza infection (17) are themselves major producers of numerous proinflammatory cytokines (47), regulated at least in part by the autonomic nervous system (48,49).…”

Section: Discussionmentioning

confidence: 99%

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Sugiyama

Gamage

Zyla

et al. 2016

J Virol

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Lung injury after influenza infection is characterized by increased permeability of the lung microvasculature, culminating in acute respiratory failure. Platelets interact with activated endothelial cells and have been implicated in the pathogenesis of some forms of acute lung injury. Autopsy studies have revealed pulmonary microthrombi after influenza infection, and epidemiological studies suggest that influenza vaccination is protective against pulmonary thromboembolism; however, the effect of influenza infection on platelet-endothelial interactions is unclear. We demonstrate that endothelial infection with both laboratory and clinical strains of influenza virus increased the adhesion of human platelets to primary human lung microvascular endothelial cells. Platelets adhered to infected cells as well as to neighboring cells, suggesting a paracrine effect. Influenza infection caused the upregulation of von Willebrand factor and ICAM-1, but blocking these receptors did not prevent platelet-endothelial adhesion. Instead, platelet adhesion was inhibited by both RGDS peptide and a blocking antibody to platelet integrin ␣ 5 ␤ 1 , implicating endothelial fibronectin. Concordantly, lung histology from infected mice revealed viral dose-dependent colocalization of viral nucleoprotein and the endothelial marker PECAM-1, while platelet adhesion and fibronectin deposition also were observed in the lungs of influenza-infected mice. Inhibition of platelets using acetylsalicylic acid significantly improved survival, a finding confirmed using a second antiplatelet agent. Thus, influenza infection induces platelet-lung endothelial adhesion via fibronectin, contributing to mortality from acute lung injury. The inhibition of platelets may constitute a practical adjunctive strategy to the treatment of severe infections with influenza. Here, we show that this infection causes platelets to adhere to the lung endothelium. Importantly, blocking platelets using two distinct antiplatelet drugs improved survival in a mouse model of severe influenza infection. Thus, platelet inhibition may constitute a novel therapeutic strategy to improve the host response to severe infections with influenza.

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Section: Discussionmentioning

confidence: 99%

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Sugiyama

Gamage

Zyla

et al. 2016

J Virol

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“…Influenza viruses, especially H5N1 strains, have been shown to induce proinflammatory cytokines in murine and human blood-monocyte-derived macrophages (20), porcine alveolar macrophage (21), transformed bronchial epithelial cell line (22), and human primary alveolar and bronchiolar epithelial cells (23). In this study, in response to H5N1 and H1N1 infections, proinflammatory cytokines IL-1β, IL-6, and TNF-α were up-regulated at mRNA level in early phase (at 6 h) as well as in late phase (at 24 h) of infection in microglia and astrocytes ( Figure 7).…”

Section: Discussionmentioning

confidence: 99%

Apoptosis and Proinflammatory Cytokine Responses of Primary Mouse Microglia and Astrocytes Induced by Human H1N1 and Avian H5N1 Influenza Viruses

Wang

Zhang

et al. 2008

Cell Mol Immunol

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Patients with an influenza virus infection can be complicated by acute encephalopathy and encephalitis. To investigate the immune reactions involved in the neurocomplication, mouse microglia and astrocytes were isolated, infected with human H1N1 and avian H5N1 influenza viruses, and examined for their immune responses. We observed homogeneously distributed viral receptors, sialic acid (SA)-α2,3-Galactose (Gal) and SA-α2,6-Gal, on microglia and astrocytes. Both viruses were replicative and productive in microglia and astrocytes. Virus-induced apoptosis and cytopathy in infected cells were observed at 24 h post-infection (p.i.). Expression of IL-1β, IL-6 and TNF-α mRNA examined at 6 h and 24 h p.i. was up-regulated, and their expression levels were considerably higher in H5N1 infection. The amounts of secreted proinflammatory IL-1β, IL-6 and TNF-α at 6 h and 24 h p.i. were also induced, with greater induction by H5N1 infection. This study is the first demonstration that both human H1N1 and avian H5N1 influenza viruses can infect mouse microglia and astrocytes and induce apoptosis, cytopathy, and proinflammatory cytokine production in them in vitro. Our results suggest that the direct cellular damage and the consequences of immunopathological injury in the CNS contribute to the influenza viral pathogenesis. Cellular & Molecular Immunology. 2008;5(2):113-120.

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“…Infection of bronchial epithelial cells by influenza A virus induces expression of interleukins IL-6, IL-8 and RANTES [1,10,22,23] which attract monocytes, T lymphocytes, eosinophils and basophils, contributing to the development of airway inflammatory disease. Alveolar epithelial cells infected by respiratory syncitial virus contribute to acute episodes of respiratory obstruction [29,33] and infected cell lines show increased expression of both intracellular -and vascular cell -adhesion molecules (ICAM-1 and VCAM-1, respectively) which contribute to inflammatory cell adherence [4,33].…”

Section: Introductionmentioning

confidence: 99%

Immortalized goat milk epithelial cell lines replicate CAEV at high level

et al. 2001

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-Primary milk epithelial cells were isolated from CAEV-uninfected goats and three cell lines designated TIGMEC-1, TIGMEC-2 and TIGMEC-3 were established. The three cell lines retained their morphological characteristics of epithelial cells and expressed specific epithelial cytokeratin marker as well as the immortalizing SV40 large T antigen. The kinetics of growth of TIGMEC1, TIG-MEC2 and TIGMEC3 cell lines showed a doubling time of 24-48 hours while the parental cell lines became senescent after the passage 6 in cell culture. Like the parental primary cells, the three cell lines were found to be highly sensitive to CAEV-pBSCA, an infectious molecular clone of CAEV-CO strain, and to a French isolate CAEV-3112. TIGMEC cell lines infected with CAEV-pBSCA became chronically infected producing high virus titers in absence of cytopathic effects. These cell lines may be useful for study of the possible physiological alterations in mammary epithelial cells infected with small ruminant lentiviruses and their consequences on milk quality. On an other hand, these cell lines can be used to study their role in virus transmission and pathogenesis. CAEV / replication / epithelial cell lineRésumé -Des cellules épithéliales du lait immortalisées répliquent le CAEV avec une grande efficacité. Des cellules épithéliales primaires isolées à partir de chèvres non infectées par le CAEV ont été immortalisées pour dériver 3 lignées appelées TIGMEC-1, TIGMEC-2 et TIGMEC-3. Les cellules des 3 lignées ont conservé leurs caractéristiques morphologiques de cellules épithéliales et expriment la cytokératine, un marqueur spécifique des cellules épithéliales et l'antigène immortalisant T du virus SV40. La courbe de croissance des lignées TIGMEC-1, TIGMEC-2 et TIGMEC-3 montre une multiplication des cellules toutes les 24 à 48 heures alors que les cellules parentales ne Vet. Res. 32 (2001) 429-440 429

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Expression of Cytokines on Human Bronchial Epithelial Cells Induced by Influenza Virus A

Cited by 76 publications

References 4 publications

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Apoptosis and Proinflammatory Cytokine Responses of Primary Mouse Microglia and Astrocytes Induced by Human H1N1 and Avian H5N1 Influenza Viruses

Immortalized goat milk epithelial cell lines replicate CAEV at high level

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