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. 2014 Apr 23;3(6):745–759. doi: 10.5966/sctm.2013-0200

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Figure 7. — Schema illustrating the crosstalk between β2-ARs and TLR2 in BM-MSCs and NHKs. Inflammatory effects of EPI and TLR2 ligands are mediated through phosphorylation of BARK-1 and engagement of MyD88, respectively, leading to decreased cell migration and increased IL-6 secretion. In addition, TLR2 ligands also induce catecholamine secretion by increasing TH and PNMT levels in BM-MSCs and NHKs, paving way for an autocrine inflammatory loop. Blocking β2-ARs with selective (ICI 118,551) or nonselective (Timolol) antagonists can reverse some effects. Abbreviations: β2AR, β2-adrenergic receptor; BARK, β-adrenergic receptor-activated kinase; Epi, epinephrine; HKSA, heat-killed Staphylococcus aureus; ICI, ICI-118,551; IL-6, interleukin-6; MALP2, macrophage-activating lipopeptide-2; NE, norepinephrine; PNMT, phenylethanolamine N-methyltransferase; TLRs, Toll-like receptors.