Abstract
BackgroundThe bacterial pathogen Streptococcus pneumoniae colonizes the nasopharynx prior to causing disease, necessitating successful competition with the resident microflora. Cytokines of the IL-17 family are important in host defence against this pathogen but their effect on the nasopharyngeal microbiome is unknown. Here we analyse the influence of IL-17 on the composition and interactions of the nasopharyngeal microbiome before and after pneumococcal colonization.ResultsUsing a murine model and 16S rRNA profiling, we found that a lack of IL-17 signalling led to profound alterations in the nasal but not lung microbiome characterized by decreased diversity and richness, increases in Proteobacteria and reduction in Bacteroidetes, Actinobacteria and Acidobacteria. Following experimental pneumococcal nasal inoculation, animals lacking IL-17 family signalling showed increased pneumococcal colonization, though both wild type and knockout animals showed as significant disruption of nasal microbiome composition, with increases in the proportion of Proteobacteria, even in animals that did not have persistent colonization. Sparse correlation analysis of the composition of the microbiome at various time points after infection showed strong positive interactions within the Firmicutes and Proteobacteria, but strong antagonism between members of these two phyla.ConclusionsThese results show the powerful influence of IL-17 signalling on the composition of the nasal microbiome before and after pneumococcal colonization, and apparent lack of interspecific competition between pneumococci and other Firmicutes. IL-17 driven changes in nasal microbiome composition may thus be an important factor in successful resistance to pneumococcal colonization and potentially could be manipulated to augment host defence against this pathogen.
Highlights
The bacterial pathogen Streptococcus pneumoniae colonizes the nasopharynx prior to causing disease, necessitating successful competition with the resident microflora
In this site as well, the resident microbiome will influence the ability of the pneumococcus to cause disease, and as with the nasopharynx, the composition of the lung microbiome will potentially be altered by specific immune mechanisms
Using 16S ribosomal DNA sequencing, we show that lack of IL-17 signalling produces profound effects on the nasopharyngeal but not the lung microbiome, with a loss in richness and diversity, expansion of Proteobacteria, and decreased abundance of Bacteroidetes and Acidobacteria
Summary
The bacterial pathogen Streptococcus pneumoniae colonizes the nasopharynx prior to causing disease, necessitating successful competition with the resident microflora. Spread of the pathogen from the site of colonization in the nasopharynx to the lower airways is thought to proceed by micro-aspiration [10, 11] In this site as well, the resident microbiome will influence the ability of the pneumococcus to cause disease, and as with the nasopharynx, the composition of the lung microbiome will potentially be altered by specific immune mechanisms. The immune mechanisms by which IL-17 provides defence against pneumococcal colonization have been well described, no studies have been made of the effects of this cytokine on the nasopharyngeal and lung microbiome before and after pneumococcal colonization Changes in these bacterial populations will influence whether an invading pneumococcal strain can compete with the resident microflora and become an established colonizer, and how rapidly it will be cleared. Pneumococcal bacteriocins can kill related bacterial species such as Micrococcus and Lactococcus species [22]; the biological importance of such activity in establishing colonization is not clear
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