Intracellular colocalization of galectin-3 with Listeria monocytogenes in macrophages and its implications (37.45)

Abstract

Abstract Galectin-3 is a β-galactoside-binding animal lectin expressed in epithelial cells and various immune cell types. In macrophages, It has been shown to be a positive regulator for FcγR-mediated phagocytosis and a negative regulator for LPS-mediated inflammation. However, its role in macrophages during infection process remains unclear. Here we investigated the role of galectin-3 in macrophages during the infection of a Gram-positive bacterium, Listeria monocytogenes (LM). Survival of LM in galectin-3-deficient (gal3-/-) bone marrow-derived macrophages (BMM) was impaired compared to that in galectin-3 wild-type (gal3+/+) BMM. This was not due to a difference in the production of bactericidal mediators nitric oxide and superoxide anion, nor a difference in the efficiency of LM escape from phagosomes between gal3+/+ or gal3-/- BMM. Interestingly, by immunofluorescence staining we detected colocalization of intracellular galectin-3 with LM at as early as 15 min after infection. The colocalization proportion peaked at 30 min post-infection, coinciding with the timing of LM escape. In vitro incubation of LM with recombinant galectin-3 was shown to promote LM growth. Based on these findings, we hypothesize that LM utilizes intracellular galectin-3 to improve its own survival and growth after escape into the host cytosol.