Macrophages as drivers of an opportunistic infection
Authors:Annette C. Vergunst1, Nazareth Lopez Carranza1, Lili Zhang1,2, Margarida C. Gomes1, Yara Tasrini1,
Annemarie H. Meijer3 and David O’Callaghan1
doi: 10.15698/mic2017.10.595
Volume 4, pp. 362 to 364, published 13/09/2017.
1 VBMI, INSERM, Univ. Montpellier, Nîmes, France.
2 Current address: Section of Molecular Biology, Division of Biological Sciences, University of California, San Diego, La Jolla, USA.
3 Institute of Biology Leiden, Leiden University, Leiden, The Netherlands.
Keywords:
Burkholderia cenocepacia, macrophages, intracellular bacteria, biofilms, opportunistic infections, cystic fibrosis, zebrafish, nosocomial infections.
Corresponding Author(s):
Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Please cite this article as: Annette C. Vergunst, Nazareth Lopez Carranza, Lili Zhang, Margarida C. Gomes, Yara Tasrini, Annemarie H. Meijer, David O’Callaghan (2017). Macrophages as drivers of an opportunistic infection. Microbial Cell 4(10): 362-364. doi: 10.15698/mic2017.10.595
© 2017 Vergunst et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Opportunistic pathogens are a worldwide cause of mortality and morbidity, and infections with intrinsically antibiotic-resistant pathogens have a large clinical, social and economic impact. Bacteria belonging to the Burkholderia cepacia complex (Bcc), ubiquitous in natural and industrial environments, are notorious pathogens for individuals with cystic fibrosis (CF). In addition, Burkholderia cenocepacia is emerging as the culprit of non-CF related, sometimes fatal infections. Knowledge of the underlying infection mechanism of these pathogens is important for efficient treatment, however, to date not much is known about the lifestyle of Bcc bacteria during infection. In our recent study published in PLoS Pathogens, we provide experimental evidence that macrophages are critically important for proliferation of B. cenocepacia, and are major drivers of fatal pro-inflammatory infections in zebrafish larvae. This is in agreement with recent clinical information showing that B. cenocepacia is mainly localised in phagocytes in infected CF lungs. A predominant intramacrophage stage and a host-detrimental role for macrophages have major implications for treatment strategies of both CF and non-CF infections. Intracellular survival of bacteria traditionally classified as extracellular, including Staphylococcus aureus and Pseudomonas aeruginosa, is an emerging theme. Our finding that macrophages are essential for proliferation of B. cenocepacia in the host suggests a new paradigm for Bcc infections and urges the development of novel anti-infectious therapies to efficiently disarm these intrinsically antibiotic resistant facultative intracellular pathogens.