TLR2-activated LSK cells produce PGE₂, and PGE₂ stimulation of LSK cells results in granulocyte differentiation in the absence of infection. (A) FACS lineage-negative, c-kit, and Sca-1–positive LSK cells were incubated in vitro with the TLR2 agonist Pam₃CSK₄ or vehicle control, and PGE₂ in culture supernatant was measured at 72 hours by enzyme-linked immunosorbent assay. Data represent 3 mice per group during 3 experiments. (B) BM LSK cells derived from CD45.2⁺-deficient, WT, TLR2-deficient, or MyD88-deficient mice were incubated with PGE₂ and were transferred to the uninfected wounds of CD45.1⁺ mice. The donor-derived CD45.1⁺-PMN number from the wounds of the respective recipient mice was enumerated by flow cytometry and was plotted relative to the untreated WT LSK cells all in saline-treated wounds 7 days after transfer. Data represent 4 mice per group. All data shown as mean ± SEM (*P < .05; **P < .01).