Francisella tularensis regulates the expression of the amino acid transporter SLC1A5 in infected THP-1 human monocytes.

摘要: Summary Francisella tularensis, a Gram-negative bacterium that causes the disease tularemia in large number of animal species, is thought to reside preferentially within macrophages vivo. F. tularensis has developed mechanisms rapidly escape from phagosome into cytoplasm infected cells, habitat with rich supply nutrients, ideal for multiplication. SLC1A5 neutral amino acid transporter expressed by human which serves, along SLC7A5 equilibrate cytoplasmic pools. We herein analysed whether was involved intracellular demonstrate expression specifically upregulated THP-1 monocytes. Furthermore, we show downregulation decreases bacterial multiplication, supporting involvement infection. Notably, after entry cells and during whole infection, highly glycosylated form deglycosylated only bacteria capable cytosolic These data suggest replication depends on function host cell SLC1A5. Our results are first, Francisella multiplication monocyte associated post-translational modification eukaryotic transporter.