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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Microcirculation. 2016 Oct;23(7):558–570. doi: 10.1111/micc.12307

Figure 7.

Figure 7

Model describing the inhibition of lymphatic contractility in the MetSyn as a consequence of inflammation. Mesenteric lymphatic vessels are constantly regulating the flux of inflammatory macrophages into the tissue through MCP1 and MCSF expression. High fructose induces alterations in the gut microbiome and elevations in dietary endotoxin that travels through the mesenteric lymph. Activation of TLR4 on lymphatic tissue results in increased expression of CCL2 and a dramatic up-regulation of GMCSF and recruitment of macrophages into the perivascular tissue and mesenteric collecting lymphatic vessels. Changes in GMCSF, inflammatory cytokines, and dietary endotoxin promote the pro-inflammatory M1 macrophage phenotype and increase iNOS expression.