ST2 gene deficiency alleviates acute gastric injury in mice by modulating inflammation and epithelial cell death

Figure 5 Suppression of tumorigenicity 2 gene deficiency attenuates neutrophil and macrophage activation and reduces gene expression of nuclear factor kappa B and NOD-like receptor family, pyrin domain containing 3. A-D: Total count of neutrophils (Ly6G+) (A) in gastric tissue following ethanol administration, along with neutrophil subsets expressing NOD-like receptor family, pyrin domain containing 3 (NLRP3) (B), expressing C-X-C motif chemokine receptor 5 and C-X-C motif chemokine receptor 4 (C), and producing tumor necrosis factor-α, interferon-γ, and interleukin-1β (D); E: Total count of macrophages (F4/80+) in gastric tissue following ethanol exposure, including M1 macrophage subsets expressing NLRP3 and producing interleukin-1β. All parameters were analyzed by flow cytometry; F and G: The mRNA expression levels of NLRP3, caspase-1 (F), and nuclear factor kappa B (G) in gastric tissue detected by real-time quantitative reverse transcriptase polymerase chain reaction. Data are presented as mean ± SEM; n = 10 mice per group. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. WT: Wild type; ST2: Suppression of tumorigenicity 2; NLRP3: NOD-like receptor family, pyrin domain containing 3; CXCR: C-X-C motif chemokine receptor; TNF-α: Tumor necrosis factor-α; IL: Interleukin; NF-κB: Nuclear factor kappa B.