Fig. 5: IL-6-driven FasL contributed to epithelial apoptosis via Fas in PHG.

a Fas, FasL staining and TUNEL staining from the indicated gastric tissues were revealed (brown, × 400, n = 6 per group). b Double staining of Fas (green) and TUNEL (red) indicated that Fas-mediated apoptosis contributed to PHG, nuclei (blue) were counterstained with DAPI (× 800, n = 6 per group). c Co-staining of Fas (green) and cytokeratin (red) demonstrated that Fas mainly located in the epithelial cells of both PHG patients and mice, nuclei (blue) were counterstained with DAPI (× 800, n = 6 per group). d Flow cytometric analysis of primary myeloid and epithelial cells isolated from SO (sham operation)- and PVL-treated mice with anti-Fas or anti-FasL antibodies (n = 6 per group). e Western blotting showed that Fas, FasL and cleaved caspase-3 were enhanced in total mucosa of PHG sections (left panel). The levels of Fas, FasL and cleaved caspase-3 in the primary myeloid and epithelial cells dissociated from PHG patients and healthy volunteers (as Un, uninvolved) were determined (right panel). β-actin was used as the loading control. n = 6 per group. f Fas, FasL and cleaved caspase-3 were enhanced in PVL-treated sections. The expressions of Fas, FasL and cleaved caspase-3 in the primary myeloid and epithelial cells dissociated from SO- and PVL-treated mice were determined (right panel). β-actin was used as the loading control. n = 6 per group