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. Author manuscript; available in PMC: 2017 Jan 1.
Published in final edited form as: J Immunol. 2015 Nov 23;196(1):428–436. doi: 10.4049/jimmunol.1501688

Figure 3. TRPV4 mediates LPS-stimulated macrophage phagocytosis of IgG-coated latex beads in vitro.

Figure 3

BMDMs or freshly-isolated alveolar macrophages were incubated ± LPS (100 ng/mL, 6-24 h) ± other indicated molecules and then incubated with IgG-coated latex beads (1.5 h). Phagocytosis was measured as signal intensity/cell. (A) Representative photomicrographs of BMDMs given IgG-coated beads ± LPS ± 30 µM HC. Green- beads, Blue- nuclei, Red- CD45 to show plasma membrane (B) Quantification of signal intensity from panel A (*,+p < 0.05). (C) Representative photomicrographs of BMDMs given IgG-coated beads ± LPS in TRPV4 siRNA-treated and TRPV4 KO cells. (D) Quantification of signal intensity from panel C (*,+p < 0.05). (E) Representative photomicrographs of alveolar macrophages (AM) given IgG-coated beads ± LPS ± HC. (F) Quantification of signal intensity from panel E (*,+p < 0.05). WT denotes WT cells in the absence of HC, WT+HC denotes WT cells in the presence of the TRPV4 inhibitor (HC). + denotes the increase by LPS vs UT, * denotes difference in LPS response as compared to WT (D) ± TRPV4 inhibitor (B,F; HC). n ≥ 3 times in at least duplicate. All photomicrograph panels, 40X Orig. Mag., scale bar 30 µm.