RESEARCH ARTICLE
The Murine Lung Microbiome Changes During Lung Inflammation and Intranasal Vancomycin Treatment
Kenneth Klingenberg Barfod1, *, Katleen Vrankx2, Hengameh Chloé Mirsepasi-Lauridsen3, Jitka Stilund Hansen1, Karin Sørig Hougaard1, Søren Thor Larsen1, Arthur C. Ouwenhand4, Karen Angeliki Krogfelt3
Article Information
Identifiers and Pagination:
Year: 2015Volume: 9
First Page: 167
Last Page: 179
Publisher ID: TOMICROJ-9-167
DOI: 10.2174/1874285801509010167
Article History:
Received Date: 24/3/2015Revision Received Date: 1/9/2015
Acceptance Date: 2/9/2015
Electronic publication date: 3/11/2015
Collection year: 2015
open-access license: This is an open access article licensed under the terms of the (https://creativecommons.org/licenses/by/4.0/legalcode), which permits unrestricted, noncommercial use, distribution and reproduction in any medium, provided the work is properly cited.
Abstract
Most microbiome research related to airway diseases has focused on the gut microbiome. This is despite advances in culture independent microbial identification techniques revealing that even healthy lungs possess a unique dynamic microbiome. This conceptual change raises the question; if lung diseases could be causally linked to local dysbiosis of the local lung microbiota. Here, we manipulate the murine lung and gut microbiome, in order to show that the lung microbiota can be changed experimentally. We have used four different approaches: lung inflammation by exposure to carbon nano-tube particles, oral probiotics and oral or intranasal exposure to the antibiotic vancomycin. Bacterial DNA was extracted from broncho-alveolar and nasal lavage fluids, caecum samples and compared by DGGE. Our results show that: the lung microbiota is sex dependent and not just a reflection of the gut microbiota, and that induced inflammation can change lung microbiota. This change is not transferred to offspring. Oral probiotics in adult mice do not change lung microbiome detectible by DGGE. Nasal vancomycin can change the lung microbiome preferentially, while oral exposure does not. These observations should be considered in future studies of the causal relationship between lung microbiota and lung diseases.
