| First Author | Shinde A | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 497 |
| Issue | 2 | Pages | 700-704 |
| PubMed ID | 29458021 | Mgi Jnum | J:270921 |
| Mgi Id | MGI:6276738 | Doi | 10.1016/j.bbrc.2018.02.135 |
| Citation | Shinde A, et al. (2018) Increased mortality from influenza infection in long-chain acyl-CoA dehydrogenase knockout mice. Biochem Biophys Res Commun 497(2):700-704 |
| abstractText | We previously showed that the mitochondrial fatty acid oxidation enzyme long-chain acyl-CoA dehydrogenase (LCAD) is expressed in alveolar type II pneumocytes and that LCAD-/- mice have altered breathing mechanics and surfactant defects. Here, we hypothesized that LCAD-/- mice would be susceptible to influenza infection. Indeed, LCAD-/- mice demonstrated increased mortality following infection with 2009 pandemic influenza (A/CA/07/09). However, the mortality was not due to increased lung injury, as inflammatory cell counts, viral titers, and histology scores all showed non-significant trends toward milder injury in LCAD-/- mice. To confirm this, LCAD-/- were infected with a second, mouse-adapted H1N1 virus (A/PR/8/34), to which they responded with significantly less lung injury. While both strains become increasingly hypoglycemic over the first week post-infection, LCAD-/- mice lose body weight more rapidly than wild-type mice. Surprisingly, while acutely fasted LCAD-/- mice develop hepatic steatosis, influenza-infected LCAD-/- mice do not. They do, however, become more hypothermic than wild-type mice and demonstrate increased blood lactate values. We conclude that LCAD-/- mice succumb to influenza from bioenergetic starvation, likely due to increased reliance upon glucose for energy. |
