Dataset Information

Upper respiratory tract metagenome

ABSTRACT: Ferret URT Targeted Locus

PROVIDER: PRJNA76689 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR388923.fastq.gz	Fastqsanger.gz
	SRR388924.fastq.gz	Fastqsanger.gz
	SRR388925.fastq.gz	Fastqsanger.gz
	SRR388926.fastq.gz	Fastqsanger.gz
	SRR388927.fastq.gz	Fastqsanger.gz

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Project description:Streptococcus pneumoniae (Spn) asymptomatically colonizes the upper respiratory tract (URT), which serves as a niche from which it can transmit to another host or cause invasive disease in the same host. While previous studies have modeled pneumococcal gene expression under infection-relevant conditions, the in vivo transcriptional adaptations that occur during nasopharyngeal colonization, particularly during influenza A virus (IAV) coinfection, are poorly understood. Here, we leveraged an established infant mouse model of colonization, shedding, and transmission to perform genome-wide transcriptomic profiling of Spn during early (day 1) and late (day 8) URT colonization and during IAV coinfection. Compared with broth-grown controls, pneumococci isolated from the URT exhibited distinct transcriptional programs, with over 200 genes differentially expressed across time points. Genes involved in carbohydrate uptake and metabolism, glycan degradation, amino sugar and nucleotide sugar metabolism, and amino acid biosynthesis were consistently enriched during colonization, highlighting metabolic adaptation to the nasopharyngeal niche. In contrast, IAV coinfection induced a markedly distinct transcriptional signature, including upregulation of branched-chain amino acid biosynthesis, bacteriocin production, and phosphate acquisition systems. Notably, the pilus islet-1 locus was upregulated during Spn-IAV coinfection. Functional studies demonstrated that while the pilus was dispensable for colonization under mono- and coinfection conditions, it promoted high-shedding events and enhanced inflammatory responses during IAV coinfection. However, reduced inflammation and reduced high shedding events from pups inoculated with a pilus-deficient mutant did not alter transmission frequency in the infant mouse model. Collectively, our findings define the in vivo transcriptional landscape of Spn during URT colonization and reveal distinct bacterial adaptations during viral coinfection, providing insight into mechanisms that influence pneumococcal persistence, inflammation, and transmission.

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Upper respiratory tract metagenome

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