Christian Rosas-Salazar1, Meghan H Shilts2, Andrey Tovchigrechko3, Seth Schobel3, James D Chappell4, Emma K Larkin5, Tebeb Gebretsadik6, Rebecca A Halpin7, Karen E Nelson8, Martin L Moore9, Larry J Anderson9, R Stokes Peebles5, Suman R Das10, Tina V Hartert11. 1. Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tenn; Center for Asthma Research, Vanderbilt University School of Medicine, Nashville, Tenn. 2. Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn; Infectious Disease Group, J. Craig Venter Institute, Rockville, Md; Infectious Disease Group, J. Craig Venter Institute, La Jolla, Calif. 3. Bioinformatics Group, J. Craig Venter Institute, Rockville, Md. 4. Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tenn. 5. Center for Asthma Research, Vanderbilt University School of Medicine, Nashville, Tenn; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn. 6. Center for Asthma Research, Vanderbilt University School of Medicine, Nashville, Tenn; Department of Biostatistics, Vanderbilt University School of Medicine, Nashville, Tenn. 7. Infectious Disease Group, J. Craig Venter Institute, Rockville, Md. 8. Genomic Medicine Group, J. Craig Venter Institute, La Jolla, Calif. 9. Center for Asthma Research, Vanderbilt University School of Medicine, Nashville, Tenn; Department of Pediatrics, Emory University School of Medicine, Atlanta, Ga. 10. Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn; Infectious Disease Group, J. Craig Venter Institute, Rockville, Md; Infectious Disease Group, J. Craig Venter Institute, La Jolla, Calif. Electronic address: suman.r.das@vanderbilt.edu. 11. Center for Asthma Research, Vanderbilt University School of Medicine, Nashville, Tenn; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn. Electronic address: tina.hartert@vanderbilt.edu.
Abstract
BACKGROUND: Early life acute respiratory infection (ARI) with respiratory syncytial virus (RSV) has been strongly associated with the development of childhood wheezing illnesses, but the pathways underlying this association are poorly understood. OBJECTIVE: To examine the role of the nasopharyngeal microbiome in the development of childhood wheezing illnesses following RSV ARI in infancy. METHODS: We conducted a nested cohort study of 118 previously healthy, term infants with confirmed RSV ARI by RT-PCR. We used next-generation sequencing of the V4 region of the 16S ribosomal RNA gene to characterize the nasopharyngeal microbiome during RSV ARI. Our main outcome of interest was 2-year subsequent wheeze. RESULTS: Of the 118 infants, 113 (95.8%) had 2-year outcome data. Of these, 46 (40.7%) had parental report of subsequent wheeze. There was no association between the overall taxonomic composition, diversity, and richness of the nasopharyngeal microbiome during RSV ARI with the development of subsequent wheeze. However, the nasopharyngeal detection and abundance of Lactobacillus was consistently higher in infants who did not develop this outcome. Lactobacillus also ranked first among the different genera in a model distinguishing infants with and without subsequent wheeze. CONCLUSIONS: The nasopharyngeal detection and increased abundance of Lactobacillus during RSV ARI in infancy are associated with a reduced risk of childhood wheezing illnesses at age 2 years.
BACKGROUND: Early life acute respiratory infection (ARI) with respiratory syncytial virus (RSV) has been strongly associated with the development of childhood wheezing illnesses, but the pathways underlying this association are poorly understood. OBJECTIVE: To examine the role of the nasopharyngeal microbiome in the development of childhood wheezing illnesses following RSVARI in infancy. METHODS: We conducted a nested cohort study of 118 previously healthy, term infants with confirmed RSVARI by RT-PCR. We used next-generation sequencing of the V4 region of the 16S ribosomal RNA gene to characterize the nasopharyngeal microbiome during RSVARI. Our main outcome of interest was 2-year subsequent wheeze. RESULTS: Of the 118 infants, 113 (95.8%) had 2-year outcome data. Of these, 46 (40.7%) had parental report of subsequent wheeze. There was no association between the overall taxonomic composition, diversity, and richness of the nasopharyngeal microbiome during RSVARI with the development of subsequent wheeze. However, the nasopharyngeal detection and abundance of Lactobacillus was consistently higher in infants who did not develop this outcome. Lactobacillus also ranked first among the different genera in a model distinguishing infants with and without subsequent wheeze. CONCLUSIONS: The nasopharyngeal detection and increased abundance of Lactobacillus during RSVARI in infancy are associated with a reduced risk of childhood wheezing illnesses at age 2 years.
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