Kupffer cells modulate hepatic fatty acid oxidation during infection with PR8 influenza
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- 作者：Tatyana N. Tarasenkoa ; Larry N. Singhb ; Milani Chatterji-Lena ; Patricia M. Zerfasc ; Kristina Cusmano-Ozogd ; Peter J. McGuirea ; peter.mcguire@nih.gov" class="auth_mail" title="E-mail the corresponding author
- 关键词：PR8 ; influenza A/PR/8 ; IEM ; inborn errors of metabolism ; OA ; organic acidemia ; UCD ; urea cycle disorder ; pMD ; primary mitochondrial disease ; TCID ; tissue culture infective dose ; MDCK ; Madin&ndash ; Darby canine kidney epithelial cells ; NS1 ; influenza non-structural protein ; CPT2 ; carnitine palmitoyl transferase 2 ; CACT ; carnitine acylcarnitine translocase ; Acadvl ; very long chain acyl CoA dehydrogenase ; Acadl ; long chain acyl CoA dehydrogenase ; Hadha ; hydroxy acyl CoA dehydrogenase ; Etfa ; electron
- 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- 出版年：2015
- 出版时间：November 2015
- 年：2015
- 卷：1852
- 期：11
- 页码：2391-2401
- 全文大小：1815 K
文摘
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During influenza infection hepatic 尾-oxidation of fatty acids is depressed.
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Concomitantly, the liver develops a significant innate anti-viral immune response.
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Kupffer cells increase in number and produce inflammatory cytokines that inhibit 尾-oxidation of fatty acids.
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Elimination of Kupffer cells with liposomal clodronate improves mRNA involved in the 尾-oxidation of fatty acids.
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The liver is lymphoid organ, which places this organ at risk for metabolic perturbations during infection, especially in IEM.