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铁酸酸化对一碳代谢和内源性病原体中毒性的合

Kendall S Stocke¹, Satya D Pandey¹, Shunying Jin¹

¹Department of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY 40202.

Proceedings of the National Academy of Sciences of the United States of America

|September 29, 2025

概括

Porphyromonas gingivalis 的毒性是由一个碳代谢 (OCM) 流量控制的. Ptk1激酶调节OCM和gingipain蛋白酶的释放,影响病原体的生存和宿主防御.

科学领域:

微生物学微生物学
分子生物学分子生物学
代谢途径代谢途径

背景情况:

内源性病原体调节宿主生存的毒性.
对微环境的代谢反应控制病原性状态,但机制尚不清楚.
一碳代谢 (OCM) 流动影响了 Porphyromonas gingivalis 的毒性.

研究的目的:

研究将OCM流与P. gingivalis毒性联系在一起的机制.
确定铁酸酸化在控制毒性因子局部化的作用.
阐明 Ptk1 激酶在 OCM 和毒性调节中的功能.

主要方法:

研究了P. gingivalis的OCM通路和氨酸酸化.
评估了pABA对Ltp1酸酶和Ptk1激酶活性的影响.
分析了gingipain蛋白酶局部化和细胞外释放.
使用动物模型来评估体内毒性.
通过Ptk1.1检查了OCM酶GlyA,GcvT和ALP的酸化.

主要成果:

pABA 抑制了 Ltp1 酸酶,激活了 Ptk1 激酶.
Ptk1的活性对于细胞外释放的gingipain蛋白酶至关重要.
缺少PABA会导致牙皮的表面保留,增强对中性粒细胞和毒性的抵抗力.
对于最大的OCM流量,需要Ptk1和gingipains.
Ptk1可化并激活OCM酶GlyA,GcvT和ALP. 这三种酶的作用.

结论:

通过控制gingipain蛋白酶局部化,Ptk1激酶对OCM平衡与毒性.
铁酸酸化调节了毒性因子的分离.
P. gingivalis利用新陈代谢调节来调整其致病潜力.

关键词:

通过BY酶.一个碳代谢的一个碳代谢.病变的发生和发病.蛋白质溶解酶是一种蛋白质溶解酶.

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