Mice Lacking Fatty Acid-Binding Protein 5 Are Resistant to Listeria monocytogenes

J Innate Immun. 2019;11(6):469-480. doi: 10.1159/000496405. Epub 2019 Mar 18.

Abstract

To investigate the role of fatty acid-binding protein 5 (FABP5) in infectious diseases, FABP5-deficient mice were challenged with Listeria monocytogenes, a facultative intracellular bacterial pathogen. Interestingly, FABP5-deficient animals were able to clear the infection within 3 days whereas control wild-type (WT) animals showed comparatively higher bacterial burdens in the liver and spleen. Sections of infected tissues showed an increase in inflammatory foci in WT mice compared to FABP5-deficient mice. FABP5-deficient mice had lower circulating inflammatory cytokines and increased inducible nitric oxide synthase production. FABP5-deficient mouse bone marrow-derived macrophages produced higher levels of nitrite anion than their WT counterparts in response to various stimuli. Additionally, in contrast to FABP5-/- mice, transgenic mice overexpressing FABP5 in myeloid cells (LysM-Cre driven) showed decreased survival rates and increased bacterial burden and inflammatory cytokines. Overall, these findings suggest that increased FABP5 levels correlate with a higher L. monocytogenes bacterial burden and elevated subsequent inflammation.

Keywords: FABP5; Listeria monocytogenes infection; Macrophages.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacterial Load
  • Cell Survival
  • Cells, Cultured
  • Cytokines / metabolism
  • Fatty Acid-Binding Proteins / genetics
  • Fatty Acid-Binding Proteins / metabolism*
  • Humans
  • Inflammation / genetics
  • Inflammation / metabolism*
  • Inflammation Mediators / metabolism
  • Listeria monocytogenes / physiology*
  • Listeriosis / genetics
  • Listeriosis / metabolism*
  • Macrophages / physiology*
  • Mice
  • Mice, Knockout
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*

Substances

  • Cytokines
  • Fabp5 protein, mouse
  • Fatty Acid-Binding Proteins
  • Inflammation Mediators
  • Neoplasm Proteins