肠道代谢物L-乳酸盐在急性感染期间支持Campylobacter jejuni的种群扩张
Ritam Sinha1, Rhiannon M LeVeque1, Sean M Callahan2
1Department of Microbiology, Genetics, & Immunology, Michigan State University, East Lansing, MI 48824.
概括
鱼中Campylobacter jejuni的殖民化揭示了乳酸盐的存在.
科学领域:
- 微生物学 微生物学
- 病变的发生和发病.
- 胃肠病学 胃肠病学
背景情况:
- 微空气病原体Campylobacter jejuni的肠道殖民机制仍然不清楚.
- 作为C. jejuni感染的自然模型,在没有免疫系统操纵的情况下反映人类疾病的进展.
- 了解C. jejuni的利基机构对于对抗食物传播疾病至关重要.
研究的目的:
- 为了调查Campylobacter jejuni在感染期间如何在肠道光线中建立其利基和繁殖.
- 阐明乳酸代谢在C. jejuni病变中的作用.
- 确定控制C. jejuni适应肠道环境的调节机制.
主要方法:
- 在C. jejuni感染研究中使用了一种模型 (Mustela putorius furo).
- 进行了组织病理学分析,观察结肠组织的变化.
- 进行了代谢分析,以量化结肠中的乳酸水平.
- 生成并测试了一种缺乏L-乳酸转运基因 (lctP) 的C. jejuni突变.
- 使用结肠癌细胞系 (HCT116) 评估C. jejuni的粘附和入侵.
主要成果:
- 在感染后2-3天内观察到C. jejuni的快速生长和肠道炎症.
- 病理生理学变化包括隐性增生,未分化的细胞的积累,以及HIF-1α的不稳定性,这表明上皮质氧化增加.
- 在感染动物的结肠中检测到高的乳酸盐含量.
- 一种C. jejuni lctP突变体表现出明显减少的殖民.
- 发现乳酸对C. jejuni的粘附和入侵有影响.
- 确定了乳酸转运体 (lctP) 的假定调节器 (LctR),在不同氧气条件下可能控制转录.
结论:
- 乳酸代谢是Campylobacter jejuni病原和肠道内殖民的一个关键因素.
- L-乳酸转运体 (lctP) 的表达与氧气可用性有关,并由LctR调节.
- 这项研究为C. jejuni在宿主肠道中壮成长和引起疾病的能力背后的机制提供了重要的见解.
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