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    Short-term consumption of a high-fat diet increases host susceptibility to Listeria monocytogenes infection

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    Author
    Heras, Vanessa L
    Clooney, Adam G
    Ryan, Feargal J
    Cabrera-Rubio, Raul
    Casey, Patrick G.
    Hueston, Cara M
    Pinheiro, Jorge
    Rudkin, Justine K
    Melgar, Silvia
    Cotter, Paul D.
    Hill, Colin
    Gahan, Cormac G M
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    Keyword
    Diet
    Infection
    Microbiome
    Listeria monocytogenes
    Mice
    Murine
    Immunity
    Goblet cell
    Date
    2019-01-18
    
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    URI
    http://hdl.handle.net/11019/1665
    Citation
    Las Heras V, Clooney AG, Ryan FJ, Cabrera-Rubio R, Casey PG, Hueston CM, Pinheiro J, Rudkin JK, Melgar S, Cotter PD and others. Short-term consumption of a high-fat diet increases host susceptibility to Listeria monocytogenes infection. Microbiome 2019;7(1):7; doi http://dx.doi.org/10.1186/s40168-019-0621-x.
    Abstract
    Background 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. Results 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. Conclusions 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.
    Funder
    European Union; Science Foundation Ireland
    Grant Number
    641984; SFI/12/RC/2273
    ae974a485f413a2113503eed53cd6c53
    https://doi.org/10.1186/s40168-019-0621-x
    Scopus Count
    Collections
    Food Biosciences
    Teagasc publications in Biomed Central

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