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Peer-reviewedCC BY-NC-ND 4.0BMC Medical Genomics

Prevotella stercorea links gut microbiome ecology to respiratory infection protection through host-context-dependent, richness-independent associations

  1. 1Stercora Biosciences Inc

Abstract

Background Using a longitudinal cohort of 633 Gambian children (IHAT-GUT, NCT02941081), we investigated two ecologically distinct pathways potentially linking Prevotella stercorea abundance to infection risk: a community-mediated pathway operating through overall gut microbiome richness, and a species-specific pathway operating independently of it. Methods We modelled P. stercorea abundance in relation to gut microbiome richness, adverse-event incidence (diarrhoea, acute respiratory infection [ARI], fever), inflammatory biomarkers (CRP, AGP; measured at enrolment [D1] only), and weight-for-age z-score (WAZ), using richness-mediation analysis, negative binomial and joint-species models, and WAZ-stratified interaction models, with Benjamini–Hochberg correction applied within each family of related tests. Results P. stercorea abundance positively predicted gut microbiome richness, consistent with a role in community-level colonisation resistance for enteric outcomes. Its association with reduced ARI persisted largely unchanged after richness adjustment, consistent with a richness-independent, species-autonomous pathway. WAZ was uncorrelated with microbiome richness within strata, consistent with WAZ serving as a proxy for host immune-metabolic reserve rather than a determinant of microbiome composition. In Low-WAZ children, P. stercorea abundance at Day 1 was associated with suppressed CRP; in High-WAZ children, elevated Day 1 inflammation predicted subsequent P. stercorea abundance at Day 85. ARI and fever protection was richness-independent and concentrated in Low-WAZ children (q≤ 0.006); P. copri did not retain an independent protective association when modelled jointly with P. stercorea (q = 0.381 vs. q = 0.016). Conclusions These findings are consistent with a richness-independent, host-context-dependent association between P. stercorea abundance and respiratory infection risk. Given the observational design, causal and mechanistic interpretations remain hypothesis-generating; experimental validation and independent replication are needed before translational application can be considered.

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BibTeX
@article{ofordile2026prevotella,
  title = {{Prevotella stercorea links gut microbiome ecology to respiratory infection protection through host-context-dependent, richness-independent associations}},
  author = {Ogochukwu Ofordile},
  journal = {BMC Medical Genomics},
  year = {2026},
  month = aug,
  doi = {10.1186/s12920-026-02449-9},
  url = {https://doi.org/10.1186/s12920-026-02449-9},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Prevotella stercorea links gut microbiome ecology to respiratory infection protection through host-context-dependent, richness-independent associations
AU  - Ogochukwu Ofordile
PY  - 2026
DA  - 2026/08/01
JO  - BMC Medical Genomics
DO  - 10.1186/s12920-026-02449-9
UR  - https://doi.org/10.1186/s12920-026-02449-9
AB  - Background Using a longitudinal cohort of 633 Gambian children (IHAT-GUT, NCT02941081), we investigated two ecologically distinct pathways potentially linking Prevotella stercorea abundance to infection risk: a community-mediated pathway operating through overall gut microbiome richness, and a species-specific pathway operating independently of it. Methods We modelled P. stercorea abundance in relation to gut microbiome richness, adverse-event incidence (diarrhoea, acute respiratory infection [ARI], fever), inflammatory biomarkers (CRP, AGP; measured at enrolment [D1] only), and weight-for-age z-score (WAZ), using richness-mediation analysis, negative binomial and joint-species models, and WAZ-stratified interaction models, with Benjamini–Hochberg correction applied within each family of related tests. Results P. stercorea abundance positively predicted gut microbiome richness, consistent with a role in community-level colonisation resistance for enteric outcomes. Its association with reduced ARI persisted largely unchanged after richness adjustment, consistent with a richness-independent, species-autonomous pathway. WAZ was uncorrelated with microbiome richness within strata, consistent with WAZ serving as a proxy for host immune-metabolic reserve rather than a determinant of microbiome composition. In Low-WAZ children, P. stercorea abundance at Day 1 was associated with suppressed CRP; in High-WAZ children, elevated Day 1 inflammation predicted subsequent P. stercorea abundance at Day 85. ARI and fever protection was richness-independent and concentrated in Low-WAZ children (q≤ 0.006); P. copri did not retain an independent protective association when modelled jointly with P. stercorea (q = 0.381 vs. q = 0.016). Conclusions These findings are consistent with a richness-independent, host-context-dependent association between P. stercorea abundance and respiratory infection risk. Given the observational design, causal and mechanistic interpretations remain hypothesis-generating; experimental validation and independent replication are needed before translational application can be considered.
SN  - 1755-8794
ER  -