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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Gastroenterology. 2014 Jan 28;146(5):1266–1277.e9. doi: 10.1053/j.gastro.2014.01.051

Figure 6. Expression of VCAM-1 by HEF and HEMC in response to cytokines and eosinophil sonicates and after blockade of signaling pathways.

Figure 6

6A: HEF and HEMC were cultured for 72 h with or without cytokines involved in the pathogenesis of EoE or eosinophil sonicates, and expression of VCAM-1 was measured by flow cytometry. IL-4 and IL-13 enhanced the expression of VCAM-1 in HEF and HEMC, while TGF-β1 decreased the amount of VCAM-1 positive HEF. N=5 for HEF and HEMC. *p<0.05, **p<0.01 compared to untreated HEF or HEMC.

6B: HEF and HEMC were plated on glass slides and incubated as for 6A. VCAM-1 expression was assessed via fluorescent microscopy after staining with a specific anti-VCAM-1 antibody. IL-4 and IL-13 increased the expression of VCAM-1 in HEF and HEMC. Figure representative of 6 experiments. Magnification 100x.

6C: Blockade of p38MAPK and ALK5 signaling reduces eosinophil adhesiveness of HEF and HEMC in response to TGF-β1 and eosinophil sonicates. HEF and HEMC were stimulated as for 6A, and p38MAPK inhibited by SB203580 and ALK5 by SB431542. Inhibition of both pathways, alone or combined, reduced the adhesion of AML14.3D10 cells to HEF and HEMC in response to TGF-β1 or eosinophil sonicates. N=5–7 for HEF and HEMC. *p<0.05 compared to no signaling inhibitor.

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