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Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1

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Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1. / Lam, Elena; Ramke, Mirja; Warnecke, Gregor; Schrepfer, Sonja; Kopfnagel, Verena; Dobner, Thomas; Heim, Albert.

In: PLOS ONE, Vol. 10, No. 7, 2015, p. e0131201.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Lam, E, Ramke, M, Warnecke, G, Schrepfer, S, Kopfnagel, V, Dobner, T & Heim, A 2015, 'Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1', PLOS ONE, vol. 10, no. 7, pp. e0131201. https://doi.org/10.1371/journal.pone.0131201

APA

Lam, E., Ramke, M., Warnecke, G., Schrepfer, S., Kopfnagel, V., Dobner, T., & Heim, A. (2015). Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1. PLOS ONE, 10(7), e0131201. https://doi.org/10.1371/journal.pone.0131201

Vancouver

Lam E, Ramke M, Warnecke G, Schrepfer S, Kopfnagel V, Dobner T et al. Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1. PLOS ONE. 2015;10(7):e0131201. https://doi.org/10.1371/journal.pone.0131201

Bibtex

@article{cabf4a7de9954c58823df25dd8d9cb7d,
title = "Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1",
abstract = "BACKGROUND: Only a few pneumotropic types of the human adenoviruses (e.g. type B14p1) cause severe lower respiratory tract infections like pneumonia and acute respiratory distress syndrome (ARDS) even in immunocompetent patients. By contrast, many other human adenovirus (HAdV) types (e.g. HAdV-C5) are associated mainly with upper respiratory tract infections. This is in accordance with a highly physiological cell culture system consisting of differentiated primary human bronchial epithelial cells which are little susceptible for apical HAdV-C5 infections.OBJECTIVE AND METHODS: We hypothesized that a pneumotropic and highly pathogenic HAdV type infects differentiated human bronchial epithelial cells efficiently from the apical surface and also induces proinflammatory cytokines in order to establish ARDS and pneumonia. Therefore, the apical infection of differentiated primary human bronchial epithelial cells with the pneumotropic and virulent type HAdV-B14p1 was investigated in comparison to the less pneumotropic HAdV-C5 as a control.RESULTS: Binding of HAdV-B14p1 to the apical surface of differentiated human bronchial epithelial cells and subsequent internalization of HAdV DNA was 10 fold higher (p<0.01) compared to the less-pneumotropic HAdV-C5 one hour after infection. Overall, the replication cycle of HAdV-B14p1 following apical infection and including apical release of infectious virus progeny was about 1000-fold more effective compared to the non-pneumotropic HAdV-C5 (p<0.001). HAdV-B14p1 infected cells expressed desmoglein 2 (DSG2), which has been described as potential receptor for HAdV-B14p1. Moreover, HAdV-B14p1 induced proinflammatory chemokines IP-10 and I-Tac as potential virulence factors. Interestingly, IP-10 has already been described as a marker for severe respiratory infections e.g. by influenza virus A H5N1.CONCLUSIONS: The efficient {"}apical to apical{"} replication cycle of HAdV-B14p1 can promote endobronchial dissemination of the infection from the upper to the lower respiratory tract. Simultaneous induction of proinflammatory cytokines probably contributes to the high virulence of HAdV-B14p1.",
keywords = "Adenovirus Infections, Human/metabolism, Adenoviruses, Human/physiology, Bronchi/pathology, Cell Differentiation, Cell Separation, Chemokines/metabolism, Desmoglein 2/metabolism, Epithelial Cells/virology, Fluorescent Antibody Technique, Humans, Inflammation Mediators/metabolism, Virion/metabolism",
author = "Elena Lam and Mirja Ramke and Gregor Warnecke and Sonja Schrepfer and Verena Kopfnagel and Thomas Dobner and Albert Heim",
year = "2015",
doi = "10.1371/journal.pone.0131201",
language = "English",
volume = "10",
pages = "e0131201",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "7",

}

RIS

TY - JOUR

T1 - Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1

AU - Lam, Elena

AU - Ramke, Mirja

AU - Warnecke, Gregor

AU - Schrepfer, Sonja

AU - Kopfnagel, Verena

AU - Dobner, Thomas

AU - Heim, Albert

PY - 2015

Y1 - 2015

N2 - BACKGROUND: Only a few pneumotropic types of the human adenoviruses (e.g. type B14p1) cause severe lower respiratory tract infections like pneumonia and acute respiratory distress syndrome (ARDS) even in immunocompetent patients. By contrast, many other human adenovirus (HAdV) types (e.g. HAdV-C5) are associated mainly with upper respiratory tract infections. This is in accordance with a highly physiological cell culture system consisting of differentiated primary human bronchial epithelial cells which are little susceptible for apical HAdV-C5 infections.OBJECTIVE AND METHODS: We hypothesized that a pneumotropic and highly pathogenic HAdV type infects differentiated human bronchial epithelial cells efficiently from the apical surface and also induces proinflammatory cytokines in order to establish ARDS and pneumonia. Therefore, the apical infection of differentiated primary human bronchial epithelial cells with the pneumotropic and virulent type HAdV-B14p1 was investigated in comparison to the less pneumotropic HAdV-C5 as a control.RESULTS: Binding of HAdV-B14p1 to the apical surface of differentiated human bronchial epithelial cells and subsequent internalization of HAdV DNA was 10 fold higher (p<0.01) compared to the less-pneumotropic HAdV-C5 one hour after infection. Overall, the replication cycle of HAdV-B14p1 following apical infection and including apical release of infectious virus progeny was about 1000-fold more effective compared to the non-pneumotropic HAdV-C5 (p<0.001). HAdV-B14p1 infected cells expressed desmoglein 2 (DSG2), which has been described as potential receptor for HAdV-B14p1. Moreover, HAdV-B14p1 induced proinflammatory chemokines IP-10 and I-Tac as potential virulence factors. Interestingly, IP-10 has already been described as a marker for severe respiratory infections e.g. by influenza virus A H5N1.CONCLUSIONS: The efficient "apical to apical" replication cycle of HAdV-B14p1 can promote endobronchial dissemination of the infection from the upper to the lower respiratory tract. Simultaneous induction of proinflammatory cytokines probably contributes to the high virulence of HAdV-B14p1.

AB - BACKGROUND: Only a few pneumotropic types of the human adenoviruses (e.g. type B14p1) cause severe lower respiratory tract infections like pneumonia and acute respiratory distress syndrome (ARDS) even in immunocompetent patients. By contrast, many other human adenovirus (HAdV) types (e.g. HAdV-C5) are associated mainly with upper respiratory tract infections. This is in accordance with a highly physiological cell culture system consisting of differentiated primary human bronchial epithelial cells which are little susceptible for apical HAdV-C5 infections.OBJECTIVE AND METHODS: We hypothesized that a pneumotropic and highly pathogenic HAdV type infects differentiated human bronchial epithelial cells efficiently from the apical surface and also induces proinflammatory cytokines in order to establish ARDS and pneumonia. Therefore, the apical infection of differentiated primary human bronchial epithelial cells with the pneumotropic and virulent type HAdV-B14p1 was investigated in comparison to the less pneumotropic HAdV-C5 as a control.RESULTS: Binding of HAdV-B14p1 to the apical surface of differentiated human bronchial epithelial cells and subsequent internalization of HAdV DNA was 10 fold higher (p<0.01) compared to the less-pneumotropic HAdV-C5 one hour after infection. Overall, the replication cycle of HAdV-B14p1 following apical infection and including apical release of infectious virus progeny was about 1000-fold more effective compared to the non-pneumotropic HAdV-C5 (p<0.001). HAdV-B14p1 infected cells expressed desmoglein 2 (DSG2), which has been described as potential receptor for HAdV-B14p1. Moreover, HAdV-B14p1 induced proinflammatory chemokines IP-10 and I-Tac as potential virulence factors. Interestingly, IP-10 has already been described as a marker for severe respiratory infections e.g. by influenza virus A H5N1.CONCLUSIONS: The efficient "apical to apical" replication cycle of HAdV-B14p1 can promote endobronchial dissemination of the infection from the upper to the lower respiratory tract. Simultaneous induction of proinflammatory cytokines probably contributes to the high virulence of HAdV-B14p1.

KW - Adenovirus Infections, Human/metabolism

KW - Adenoviruses, Human/physiology

KW - Bronchi/pathology

KW - Cell Differentiation

KW - Cell Separation

KW - Chemokines/metabolism

KW - Desmoglein 2/metabolism

KW - Epithelial Cells/virology

KW - Fluorescent Antibody Technique

KW - Humans

KW - Inflammation Mediators/metabolism

KW - Virion/metabolism

U2 - 10.1371/journal.pone.0131201

DO - 10.1371/journal.pone.0131201

M3 - SCORING: Journal article

C2 - 26168049

VL - 10

SP - e0131201

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 7

ER -