tetano
Editor, Senior Moderator
J Virol. 2012 Mar 7. [Epub ahead of print]
PLASTICITY AND VIRUS-SPECIFICITY OF THE AIRWAY EPITHELIAL CELL IMMUNE RESPONSE DURING RESPIRATORY VIRAL INFECTION.
Ioannidis I, McNally B, Willette M, Peeples ME, Chaussabel D, Durbin JE, Ramilo O, Mejias A, Fla?o E.
Source
Center for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43205.
Abstract
Airway epithelial cells (AECs) provide the first line of defense in the respiratory tract and are the main target of respiratory viruses. Here, using oligonucleotide and protein arrays, we analyzed the infection of primary polarized human AEC cultures with influenza virus and respiratory syncytial virus (RSV), and show that the immune response of AECs was quantitatively and qualitatively virus-specific. Differentially expressed genes (DEGs) specifically induced by influenza virus and not by RSV included IFNB1, type III interferons (IL28A, IL28B and IL29), interleukins (IL6, IL1A, IL1B, IL23A, IL17C and IL32) and chemokines (CCL2, CCL8 and CXCL5). Lack of type I interferon or STAT1 signaling decreased the expression and secretion of cytokines and chemokines by the airways epithelium. We also observed a strong basolateral polarization of the secretion of cytokines and chemokines by human and murine AECs during infection. Importantly, the anti-viral response of human AECs to influenza virus or to RSV correlated with the infection signature obtained from PBMCs isolated from patients with acute influenza or RSV bronchiolitis, respectively. IFI27 (also known as ISG12) was identified as a biomarker of respiratory virus infection in both AECs and PBMCs. In addition, the extent of the transcriptional perturbation in PBMCs correlated with the clinical disease severity. Our results demonstrate that the human airway epithelium mounts virus-specific immune responses that are likely to determine the subsequent systemic immune responses, and suggest that the absence of epithelial immune mediators after RSV infection may contribute to explain the inadequacy of the systemic immunity to this virus.
PMID:
22398282
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22398282
PLASTICITY AND VIRUS-SPECIFICITY OF THE AIRWAY EPITHELIAL CELL IMMUNE RESPONSE DURING RESPIRATORY VIRAL INFECTION.
Ioannidis I, McNally B, Willette M, Peeples ME, Chaussabel D, Durbin JE, Ramilo O, Mejias A, Fla?o E.
Source
Center for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43205.
Abstract
Airway epithelial cells (AECs) provide the first line of defense in the respiratory tract and are the main target of respiratory viruses. Here, using oligonucleotide and protein arrays, we analyzed the infection of primary polarized human AEC cultures with influenza virus and respiratory syncytial virus (RSV), and show that the immune response of AECs was quantitatively and qualitatively virus-specific. Differentially expressed genes (DEGs) specifically induced by influenza virus and not by RSV included IFNB1, type III interferons (IL28A, IL28B and IL29), interleukins (IL6, IL1A, IL1B, IL23A, IL17C and IL32) and chemokines (CCL2, CCL8 and CXCL5). Lack of type I interferon or STAT1 signaling decreased the expression and secretion of cytokines and chemokines by the airways epithelium. We also observed a strong basolateral polarization of the secretion of cytokines and chemokines by human and murine AECs during infection. Importantly, the anti-viral response of human AECs to influenza virus or to RSV correlated with the infection signature obtained from PBMCs isolated from patients with acute influenza or RSV bronchiolitis, respectively. IFI27 (also known as ISG12) was identified as a biomarker of respiratory virus infection in both AECs and PBMCs. In addition, the extent of the transcriptional perturbation in PBMCs correlated with the clinical disease severity. Our results demonstrate that the human airway epithelium mounts virus-specific immune responses that are likely to determine the subsequent systemic immune responses, and suggest that the absence of epithelial immune mediators after RSV infection may contribute to explain the inadequacy of the systemic immunity to this virus.
PMID:
22398282
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22398282