Bacterial biofilms are responsible for a variety of serious human infections and are notoriously difficult to treat due to their recalcitrance to antibiotics. Further work is necessary to elicit a full understanding of the mechanism of this antibiotic tolerance. The arginine deiminase (ADI) pathway is responsible for bacterial pH maintenance and is highly expressed during biofilm growth in multiple bacterial species. Using the group A Streptococcus (GAS) as a model human pathogen, the ADI pathway was demonstrated to contribute to biofilm growth. The inability of antibiotics to reduce GAS populations when in a biofilm was demonstrated by in vitro studies and a novel animal model of nasopharyngeal infection. However, disruption of the ADI pathway returned GAS biofilms to planktonic levels of antibiotic sensitivity, suggesting the ADI pathway is influential in biofilm-related antibiotic treatment failure and provides a new strategic target for the treatment of biofilm infections in GAS and potentially numerous other bacterial species.

中文翻译：

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在生物膜介导的化脓性链球菌感染过程中，精氨酸脱亚氨酶途径影响抗生素耐受性。

细菌生物膜导致多种严重的人类感染，并且由于对抗生素的顽固性而难以治疗。为了充分理解这种抗生素耐受性的机制，有必要做进一步的工作。精氨酸脱亚氨酶（ADI）途径负责维持细菌的pH值，并在多种细菌物种的生物膜生长过程中高度表达。使用A群链球菌（GAS）作为人类模型病原体，ADI途径被证明有助于生物膜的生长。体外证明在生物膜中抗生素无法减少GAS种群研究和鼻咽感染的新型动物模型。但是，ADI途径的破坏使GAS生物膜恢复到浮游生物水平的抗生素敏感性，这表明ADI途径在生物膜相关的抗生素治疗失败中具有影响力，并为GAS和潜在的许多其他细菌物种中生物膜感染的治疗提供了新的战略目标。 。