APC Microbiome Ireland, University College Cork, Cork, Ireland.
School of Microbiology, University College Cork, Cork, Ireland.
Microbiome. 2019 Jan 18;7(1):7. doi: 10.1186/s40168-019-0621-x.
A westernized diet comprising a high caloric intake from animal fats is known to influence the development of pathological inflammatory conditions. However, there has been relatively little focus upon the implications of such diets for the progression of infectious disease. Here, we investigated the influence of a high-fat (HF) diet upon parameters that influence Listeria monocytogenes infection in mice.
We determined that short-term administration of a HF diet increases the number of goblet cells, a known binding site for the pathogen, in the gut and also induces profound changes to the microbiota and promotes a pro-inflammatory gene expression profile in the host. Host physiological changes were concordant with significantly increased susceptibility to oral L. monocytogenes infection in mice fed a HF diet relative to low fat (LF)- or chow-fed animals. Prior to Listeria infection, short-term consumption of HF diet elevated levels of Firmicutes including Coprococcus, Butyricicoccus, Turicibacter and Clostridium XIVa species. During active infection with L. monocytogenes, microbiota changes were further exaggerated but host inflammatory responses were significantly downregulated relative to Listeria-infected LF- or chow-fed groups, suggestive of a profound tempering of the host response influenced by infection in the context of a HF diet. The effects of diet were seen beyond the gut, as a HF diet also increased the sensitivity of mice to systemic infection and altered gene expression profiles in the liver.
We adopted a systems approach to identify the effects of HF diet upon L. monocytogenes infection through analysis of host responses and microbiota changes (both pre- and post-infection). Overall, the results indicate that short-term consumption of a westernized diet has the capacity to significantly alter host susceptibility to L. monocytogenes infection concomitant with changes to the host physiological landscape. The findings suggest that diet should be a consideration when developing models that reflect human infectious disease.
已知富含动物脂肪的西式饮食会影响病理性炎症的发展。然而，对于这种饮食对传染病进展的影响，关注相对较少。在这里，我们研究了高脂肪（HF）饮食对影响单核细胞增生李斯特菌感染小鼠的参数的影响。
我们确定短期给予 HF 饮食会增加肠道中杯状细胞的数量，杯状细胞是病原体的已知结合部位，并且还会对微生物群产生深远的影响，并促进宿主中促炎基因表达谱的形成。宿主生理变化与 HF 饮食喂养的小鼠相对于低脂（LF）或标准饮食喂养的动物对口腔单核细胞增生李斯特菌感染的易感性显著增加一致。在李斯特菌感染之前，短期 HF 饮食会增加厚壁菌门的水平，包括粪球菌、丁酸球菌、瘤胃球菌和梭菌 XIVa 种。在感染单核细胞增生李斯特菌期间，微生物群的变化进一步加剧，但与 LF 或标准饮食喂养的李斯特菌感染组相比，宿主炎症反应显著下调，提示在 HF 饮食背景下，感染对宿主反应的影响显著减弱。饮食的影响不仅限于肠道，因为 HF 饮食还增加了小鼠对全身感染的敏感性，并改变了肝脏的基因表达谱。
我们通过分析宿主反应和微生物群变化（感染前后），采用系统方法来确定 HF 饮食对单核细胞增生李斯特菌感染的影响。总体而言，结果表明，短期摄入西式饮食有能力显著改变宿主对单核细胞增生李斯特菌感染的易感性，同时改变宿主生理状态。研究结果表明，在开发反映人类传染病的模型时，应考虑饮食因素。
