Figure 7. Proposed role of Hedgehog-dependent myeloid cells in Helicobacter-induced gastric metaplasia.

Upon Helicobacter infection, CD11b⁺CD11c⁻Slfn-4⁻ myeloid cells migrate from the bone marrow to the stomach in response to Shh ligand secretion from parietal cells. Prolonged exposure of these cells to the inflamed gastric environment induced by H. felis (∼6 months) induces a phenotypic shift into CD11b⁺CD11c⁺ myeloid cells, which express the marker Slfn-4. Gli1 expression in myeloid cells is necessary for this shift. Myeloid cell-derived IL-1β triggers the IL-6/pSTAT-3 pathway in epithelial mucous cells leading to mucous neck cell proliferation at the expense of parietal and chief cells (gland atrophy) and metaplasia (SPEM).