Sylvia Kristyn E, Demas Gregory E
Department of Biology, Indiana University, Bloomington, Indiana.
Center for the Integrative Study of Animal Behavior, Indiana University, Bloomington, Indiana.
Physiol Rep. 2018 Mar;6(5). doi: 10.14814/phy2.13639.
There is bidirectional communication between the immune system and the gut microbiome, however the precise mechanisms regulating this crosstalk are not well understood. Microbial-associated molecular patterns (MAMPs) within the gut, including lipopolysaccharide (LPS) that produces a quick and robust activation of the immune system, may be one way by which these interactions occur. Endogenous levels of LPS in the gut are low enough that they do not usually cause disease, although, in times of increased LPS loads, they may be capable of increasing vulnerability of the gut to pathogenic bacteria. Furthermore, chronic, low-grade inflammation can have lasting effects on the gut, but the effects of acute inflammation on gut communities have not been thoroughly assessed. In this study, we first investigated whether a single modest dose of LPS administered to adult male and female Siberian hamsters (Phodopus sungorus) activated the immune system by measuring levels of circulating cortisol and the proinflammatory cytokine TNF-α in the liver compared with saline-treated animals. We then investigated whether this same acute dose of LPS altered the microbiome 48 h after treatment. We found that, although LPS increased cortisol and liver cytokine levels, and produced changes in food intake and body mass in both sexes, immunological changes were independent of gut dysbiosis 48 h after LPS injection. These data suggest that an acute immune activation may not be capable of altering the gut microbiome in healthy individuals. It is likely, however, that this type of immune challenge may have other physiological impacts on the gut's vulnerability, and future studies will investigate these relationships further.
免疫系统与肠道微生物群之间存在双向交流,然而,调节这种相互作用的精确机制尚未完全明确。肠道内的微生物相关分子模式(MAMPs),包括能快速且强烈激活免疫系统的脂多糖(LPS),可能是这些相互作用发生的一种方式。肠道内LPS的内源性水平足够低,以至于通常不会引发疾病,不过,在LPS负荷增加时,它们可能会增加肠道对病原菌的易感性。此外,慢性低度炎症会对肠道产生持久影响,但急性炎症对肠道菌群的影响尚未得到充分评估。在本研究中,我们首先通过测量与盐水处理组动物相比,成年雄性和雌性西伯利亚仓鼠(Phodopus sungorus)循环皮质醇水平以及肝脏中促炎细胞因子TNF-α水平,来研究单次适度剂量的LPS是否会激活免疫系统。然后,我们研究了相同急性剂量的LPS在处理后48小时是否会改变微生物群。我们发现,尽管LPS增加了皮质醇和肝脏细胞因子水平,并在两性中引起了食物摄入量和体重的变化,但LPS注射后48小时的免疫变化与肠道菌群失调无关。这些数据表明,急性免疫激活可能无法改变健康个体的肠道微生物群。然而,这种类型的免疫挑战可能会对肠道的易感性产生其他生理影响,未来的研究将进一步探究这些关系。