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Updated: May 18, 2026

Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
The Wingless homolog Wnt5a stimulates phagocytosis but not bacterial killing
George Maiti1, Debdut Naskar, Malini Sen
1Division of Cancer Biology and Inflammatory Disorder, Indian Institute of Chemical Biology, Jadavpur, Kolkata, India.
Abstract:
Phagocytosis is a primary defense program orchestrated by monocytes/macrophages. Unregulated phagocytosis can lead to pathological conditions. In the current study we have demonstrated that Wnt5a stimulates phagocytosis through PI3 kinase-Rac1 and lipid-raft-dependent processes. Wnt5a-mediated augmentation in phagocytosis is suppressed by blocking expression of the putative Wnt5a receptor Frizzled 5. Enhanced phagocytosis of bacteria by Wnt5a-Fz5 signaling increases the secretion of proinflammatory cytokines, but not the bacterial killing rate. Furthermore, a small molecule inhibitor of Wnt production, IWP-2, which reduces secretion of functionally active Wnt5a, not only suppresses both phagocytosis and the secretion of proinflammatory cytokines but also accelerates the bacterial killing rate.
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