کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10148346 | 1646559 | 2018 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Analysis of mycobacterial infection-induced changes to host lipid metabolism in a zebrafish infection model reveals a conserved role for LDLR in infection susceptibility
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
علوم آبزیان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Analysis of mycobacterial infection-induced changes to host lipid metabolism in a zebrafish infection model reveals a conserved role for LDLR in infection susceptibility Analysis of mycobacterial infection-induced changes to host lipid metabolism in a zebrafish infection model reveals a conserved role for LDLR in infection susceptibility](/preview/png/10148346.png)
چکیده انگلیسی
Changes to lipid metabolism are well-characterised consequences of human tuberculosis infection but their functional relevance are not clearly elucidated in these or other host-mycobacterial systems. The zebrafish-Mycobacterium marinum infection model is used extensively to model many aspects of human-M. tuberculosis pathogenesis but has not been widely used to study the role of infection-induced lipid metabolism. We find mammalian mycobacterial infection-induced alterations in host Low Density Lipoprotein metabolism are conserved in the zebrafish model of mycobacterial pathogenesis. Depletion of LDLR, a key lipid metabolism node, decreased M. marinum burden, and corrected infection-induced altered lipid metabolism resulting in decreased LDL and reduced the rate of macrophage transformation into foam cells. Our results demonstrate a conserved role for infection-induced alterations to host lipid metabolism, and specifically the LDL-LDLR axis, across host-mycobacterial species pairings.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Fish & Shellfish Immunology - Volume 83, December 2018, Pages 238-242
Journal: Fish & Shellfish Immunology - Volume 83, December 2018, Pages 238-242
نویسندگان
Matt D. Johansen, Elinor Hortle, Joshua A. Kasparian, Alejandro Romero, Beatriz Novoa, Antonio Figueras, Warwick J. Britton, Kumudika de Silva, Auriol C. Purdie, Stefan H. Oehlers,