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Original Research ARTICLE

Front. Cell. Infect. Microbiol. | doi: 10.3389/fcimb.2017.00218


Viviane Balloy1, Remya Koshy2, Lea Perra1, Harriet Corvol1, 3, Michel Chignard1, Loic Guillot1* and Vinod Scaria2, 4*
  • 1INSERM, Centre de Recherche Saint-Antoine, Paris, Sorbonne Universités, UPMC Univ Paris 06,, France
  • 2Institute of Genomics and Integrative Biology, India
  • 3Pneumologie pédiatrique, AP-HP, Hôpital Trousseau, France
  • 4Faculty of Biological Sciences, Academy of Scientific & Innovative Research, India

Pseudomonas aeruginosa (Pa) is the leading cause of chronic lung infection in Cystic Fibrosis (CF) patients. It is well recognized that CF epithelial cells fail to develop an appropriate response to infection, allowing bacterial colonization and a chronic inflammatory response. Since long non-coding RNAs (lncRNAs), are known to play a key role in regulating mammalian innate immune response, we hypothesized that CF cells exposed to Pa could express a specific lncRNA signature responsible of the maladaptative CF response. We analysed transcriptomic datasets to compare the expression profiles of lncRNAs in primary CF and non CF epithelial cells infected with Pa at 0, 2, 4 and 6 hours of infection. Our analysis identified temporal expression signatures of 25, 73, 15 and 26 lncRNA transcripts differentially expressed at 0, 2, 4 and 6 h post-infection respectively, between CF and non CF cells. In addition, we identified profiles specific to CF and non CF cells. The differential expression of two candidate lncRNAs were independently validated using real-time PCR. We identified a specific CF signature of lncRNA expression in a context of Pa infection that could potentially play a role in the maladaptive immune response of CF patients.

Keywords: Cystic Fibrosis, Lung, Epithelium, Pseudomonas aeruginosa, lncRNA, Gene Expression, Signature

Received: 02 Feb 2017; Accepted: 11 May 2017.

Edited by:

Silvia M. Uriarte, University of Louisville, United States

Reviewed by:

Gill Diamond, University of Florida, United States
Gregory Anderson, Indiana University, Purdue University Indianapolis, United States  

Copyright: © 2017 Balloy, Koshy, Perra, Corvol, Chignard, Guillot and Scaria. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Dr. Loic Guillot, Sorbonne Universités, UPMC Univ Paris 06,, INSERM, Centre de Recherche Saint-Antoine, Paris, Paris, France,
Dr. Vinod Scaria, Institute of Genomics and Integrative Biology, Delhi, India,