Journal of oral biosciences · 2025
Dextrin utilization in Streptococcus pyogenes pathogenesis and growth.
СтатьяОбзорПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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.
Hirose Yujiro, Nizet Victor, Kawabata Shigetada
Аннотация
BACKGROUND: Streptococcus pyogenes has several clinical manifestations, from mild pharyngitis to life-threatening necrotizing fasciitis. Nutrient conditions strongly influence its virulence, and the ability to metabolize dextrin contributes to growth and pathogenicity. Since dextrin-dependent phenotypes link metabolic adaptation with virulence regulation, reviewing the current knowledge is essential for understanding how carbohydrate utilization shapes S. pyogenes pathogenesis and proliferation.
HIGHLIGHT: Animal models have demonstrated that the maltose/dextrin utilization operon enhances fitness and is co-activated with major toxins at infection sites. System-level analyses have shown that dextrin induces the nga-ifs-slo operon and activates CovRS-associated modules, a regulatory system central to virulence control. Dextrin also promotes in vitro growth, with genome-scale metabolic modeling implicating increased arginine metabolism in this phenotype. Collectively, these results suggest that dextrin acts as a regulatory cue to reprogram virulence and metabolic capacity.
CONCLUSION: Dextrin utilization shapes both the growth and virulence of S. pyogenes. Although the mechanisms remain incompletely defined, integrating metabolic modeling with experimental approaches will be crucial for clarifying how carbohydrate use drives invasive diseases.
HIGHLIGHT: Animal models have demonstrated that the maltose/dextrin utilization operon enhances fitness and is co-activated with major toxins at infection sites. System-level analyses have shown that dextrin induces the nga-ifs-slo operon and activates CovRS-associated modules, a regulatory system central to virulence control. Dextrin also promotes in vitro growth, with genome-scale metabolic modeling implicating increased arginine metabolism in this phenotype. Collectively, these results suggest that dextrin acts as a regulatory cue to reprogram virulence and metabolic capacity.
CONCLUSION: Dextrin utilization shapes both the growth and virulence of S. pyogenes. Although the mechanisms remain incompletely defined, integrating metabolic modeling with experimental approaches will be crucial for clarifying how carbohydrate use drives invasive diseases.