降硫酸盐细菌通过PI3K/Akt路径以TLR双依赖的方式诱导促炎性TNF-α和iNOS
Sudha B Singh1, Cody A Braun1, Amanda Carroll-Portillo2
1Biomedical Research Institute of New Mexico, New Mexico Veterans Affairs (VA) Health Care System, 1501 San Pedro Dr. SE, Albuquerque, NM 87108, USA.
肠道细菌Desulfovibrio (DSV) 通过PI3K/Akt路径诱导瘤亡因子α (TNF-α) 和可诱导的氧化合成酶 (iNOS),依赖于托尔类受体2 (TLR2) 激活炎症.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 减少硫酸盐的细菌 (SRB),包括*Desulfovibrio*,与炎症性疾病有关.
- PI3K/Akt信号通路对于炎症反应至关重要,并且在疾病中经常失调.
- 收费类受体 (TLR) 信号可以激活细菌诱导的通路.
研究的目的:
- 通过PI3K/Akt信号传递,研究是否诱导*Desulfovibrio vulgaris* (DSV) 通过PI3K/Akt信号传递诱导促炎媒介TNF-α和iNOS.
- 要确定这种诱导是否依赖于TLR 2激活.
主要方法:
- RAW 264.7 巨细胞被DSV感染.
- 测量了关键信号分子 (p-Akt,p-p70S6K,p-NF-κB,p-IkB) 和炎症标记物 (TNF-α,iNOS) 的蛋白质表达.
- 使用特定抑制剂 (PI3K/Akt的LY294002,TL2-C29的TLR2) 来阻断路径.
主要成果:
- DSV感染导致PI3K/Akt通路激活和下游炎症蛋白质表达的时间依赖性增加.
- 无论是活的还是被热杀死的DSV,但不是培养上游生物或*Lactobacillus plantarum*,诱导PI3K/AKT/TNF/iNOS.
- PI3K/Akt和TLR 2的抑制剂阻断了DSV诱导的通路激活.
结论:
- *Desulfovibrio vulgaris*通过PI3K/Akt路径诱导促炎性TNF-α和iNOS的表达.
- 这种炎症反应以TLR2依赖的方式进行介导.
- 这项研究揭示了SRB过度生长可能导致相关疾病炎症的机制.
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