Airway epithelial cell response to human metapneumovirus infection

Xiaoyong Bao, T. Liu, L. Spetch, D. Kolli, Roberto Garofalo, Antonella Casola

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Human metapneumovirus (hMPV) is a major cause of lower respiratory tract infections (LRTIs) in infants, elderly and immunocompromised patients. In this study, we show that hMPV can infect in a similar manner epithelial cells representative of different tracts of the airways. hMPV-induced expression of chemokines IL-8 and RANTES in primary small alveolar epithelial cells (SAE) and in a human alveolar type II-like epithelial cell line (A549) was similar, suggesting that A549 cells can be used as a model to study lower airway epithelial cell responses to hMPV infection. A549 secreted a variety of CXC and CC chemokines, cytokines and type I interferons, following hMPV infection. hMPV was also a strong inducer of transcription factors belonging to nuclear factor (NF)-κB, interferon regulatory factors (IRFs) and signal transducers and activators of transcription (STATs) families, which are known to orchestrate the expression of inflammatory and immunomodulatory mediators.

Original languageEnglish (US)
Pages (from-to)91-101
Number of pages11
JournalVirology
Volume368
Issue number1
DOIs
StatePublished - Nov 10 2007

Fingerprint

Metapneumovirus
Epithelial Cells
Infection
Interferon Regulatory Factors
Alveolar Epithelial Cells
CXC Chemokines
Chemokine CCL5
CC Chemokines
Interferon Type I
Immunocompromised Host
Transducers
Interleukin-8
Chemokines
Respiratory Tract Infections
Transcription Factors
Cytokines
Cell Line

Keywords

  • Airway epithelial cells
  • Chemokines
  • hMPV
  • Inflammation
  • Transcription factors

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this

Airway epithelial cell response to human metapneumovirus infection. / Bao, Xiaoyong; Liu, T.; Spetch, L.; Kolli, D.; Garofalo, Roberto; Casola, Antonella.

In: Virology, Vol. 368, No. 1, 10.11.2007, p. 91-101.

Research output: Contribution to journalArticle

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