Abstract
Abstract Galectin-3 is a β-galactoside-binding animal lectin expressed in various immune cell types including macrophages. It has been implicated as a positive regulator of macrophage phagocytosis and as a negative regulator of LPS-mediated inflammation. However, its role in macrophage antibacterial function has not been fully elucidated. The aim of this study was to investigate the role of galectin-3 in macrophage antibacterial function against Listeria monocytogenes (LM) infection by studying bone marrow-derived macrophages (BMM) from galectin-3-deficient (gal3-/-) and wild-type (gal3+/+) mice. After in vitro infection, gal3-/- BMM contained significantly fewer viable intracellular bacteria than gal3+/+ BMM. Consistently, immunofluorescent staining of infected BMM revealed a significantly lower percentage of cytosolic LM escaped from phagosomes in gal3-/- BMM compared to gal3+/+ BMM. Higher levels of reactive nitrogen intermediate nitric oxide (NO) but lower levels of inflammatory cytokine IL-1β were detected in LM-infected gal3-/- BMM compared to gal3+/+ cells. In addition, we noted elevated levels of NAD(P)H in gal3-/- BMM which may contribute to higher amounts of NO in gal3-/- BMM. We conclude that galectin-3 plays a regulatory role in macrophage antibacterial function by interfering with the production of NO, thereby facilitating the survival and replication of intracellular bacteria.
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