bioRxiv : the preprint server for biology · 2026
Paired oral clinical specimens reveal the underlying ecology supporting the emergence of inflammophilic microbiome communities.
СтатьяПрепринтНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Krieger Madeline, Kerns Kristopher A, Palmer Elizabeth A, McLean Jeffery S, Kreth Jens, Yardimci Galip Gürkan, Merritt Justin L
Аннотация
BACKGROUND: Inflammatory oral diseases are associated with reproducible shifts from commensal-dominated microbiota toward pathobiont-enriched communities, yet the ecological mechanisms underlying the emergence of inflammophiles remain poorly understood. This study aims to investigate if host-derived inflammatory environments act as selective pressures that restructure microbial metabolism and community organization during disease progression.
METHODS: We performed 16S rRNA gene sequencing of patient-matched pediatric dental plaque and odontogenic abscess specimens to capture microbial community transitions across an inflammatory ecological gradient. Community ecology modeling and inferred metagenomic analyses were used to identify taxa and functional programs associated with commensal and inflammophilic states.
RESULTS: Patient-matched comparisons revealed a reproducible ecological selection gradient linking inflammatory environments to expansion of metabolically specialized inflammophiles and depletion of carbohydrate-utilizing commensals. Commensal-dominated plaque communities exhibited anabolic, carbohydrate-centered metabolic capacity, whereas abscess microbiota were enriched for catabolic metabolism, amino acid fermentation, and antimicrobial resistance, consistent with adaptation to inflammation-driven nutrient landscapes and immune pressure.
CONCLUSIONS: These findings support a model in which host inflammation drives ecological restructuring of the oral microbiome toward metabolically adapted inflammophilic communities. Defining the metabolic requirements and selective pressures governing these transitions provides a framework for microbiome-directed therapeutic strategies aimed at restoring ecological stability during inflammatory dysbiosis.
METHODS: We performed 16S rRNA gene sequencing of patient-matched pediatric dental plaque and odontogenic abscess specimens to capture microbial community transitions across an inflammatory ecological gradient. Community ecology modeling and inferred metagenomic analyses were used to identify taxa and functional programs associated with commensal and inflammophilic states.
RESULTS: Patient-matched comparisons revealed a reproducible ecological selection gradient linking inflammatory environments to expansion of metabolically specialized inflammophiles and depletion of carbohydrate-utilizing commensals. Commensal-dominated plaque communities exhibited anabolic, carbohydrate-centered metabolic capacity, whereas abscess microbiota were enriched for catabolic metabolism, amino acid fermentation, and antimicrobial resistance, consistent with adaptation to inflammation-driven nutrient landscapes and immune pressure.
CONCLUSIONS: These findings support a model in which host inflammation drives ecological restructuring of the oral microbiome toward metabolically adapted inflammophilic communities. Defining the metabolic requirements and selective pressures governing these transitions provides a framework for microbiome-directed therapeutic strategies aimed at restoring ecological stability during inflammatory dysbiosis.