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Environmental Modulation of Oral Treponeme Virulence in a Murine Model

机译：小鼠模型中口服三联体毒性的环境调节。

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This investigation examined the effects of environmental alteration on the virulence of the oral treponemes Treponema denticolaand Treponema pectinovorum. The environmental effects were assessed by using a model of localized inflammatory abscesses in mice. In vitro growth of T. denticola and T. pectinovorum as a function of modification of the cysteine concentration significantly enhanced abscess formation and size. In contrast, growth of T. denticola or T. pectinovorum under iron-limiting conditions (e.g., dipyridyl chelation) had no effect on abscess induction in comparison to that when the strains were grown under normal iron conditions. In vivo modulation of the microenvironment at the focus of infection with Cytodex beads demonstrated that increasing the local inflammation had no effect on lesion induction or size. In vivo studies involved the determination of the effects of increased systemic iron availability (e.g., iron dextran or phenylhydrazine) on the induction, kinetics, and size of lesions. T. denticola induced significantly larger lesions in mice with iron pretreatment and demonstrated systemic manifestations of the infectious challenge and an accompanying spreading lesion with phenylhydrazine pretreatment (e.g., increases in circulating free hemoglobin). In contrast, T. pectinovorum virulence was minimally affected by this in vivo treatment to increase iron availability. T. denticolavirulence, as evaluated by lesion size, was increased additively by in vivo iron availability, and cysteine modified growth of the microorganism. Additionally, galactosamine sensitized mice to a lethal outcome following infection with both T. denticola andT. pectinovorum, suggesting an endotoxin-like activity in these treponemes. These findings demonstrated the ability to modify the virulence capacity of T. denticola andT. pectinovorum by environmental conditions which can be evaluated by using in vivo murine models.
机译：这项研究调查了环境改变对口腔梅毒螺旋体和果胶螺旋体的致病力的影响。通过使用小鼠中的局部炎性脓肿模型评估环境影响。 Tem的体外生长。 denticola 和 T。果胶含量是半胱氨酸浓度改变的函数，明显增加了脓肿的形成和大小。相反， T的增长。 denticola 或 T。与在正常铁条件下生长的菌株相比，在铁限制条件下的果胶毒素（例如，二吡啶基螯合）对脓肿的诱导没有影响。以Cytodex磁珠感染为中心的微环境的体内调节表明，增加局部炎症对病变的诱发或大小没有影响。体内研究涉及确定全身可用铁的增加（例如右旋糖酐铁或苯肼铁）对皮损的诱发，动力学和大小的影响。 T。在铁预处理下，树突状细胞诱发小鼠明显更大的病变，并证明了感染挑战的全身表现以及苯肼预处理伴随的扩散性病变（例如，循环血红蛋白的增加）。相反， T。这种体内治疗对果胶毒素的毒力影响最小，以增加铁的利用率。 T。通过病灶大小评估，树突状病毒的毒性通过体内铁的利用和半胱氨酸修饰微生物的生长而增加。另外，半乳糖胺致敏的小鼠在两种em感染后均致死。 denticola 和 T。果胶菌素，提示这些色氨酸内毒素样活性。这些发现证明了改变 T毒力能力的能力。 denticola 和 T。通过使用体内鼠模型可以评估环境条件的果胶。

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