The Wingless homolog Wnt5a stimulates phagocytosis but not bacterial killing.

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.

authors

Maiti G,Naskar D,Sen M

doi

10.1073/pnas.1207789109

subject

Has Abstract

pub_date

2012-10-09 00:00:00

pages

16600-5

issue

41

eissn

0027-8424

issn

1091-6490

pii

1207789109

journal_volume

109

pub_type

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