Does the histamine H3 receptor agonist N alpha-methylhistamine produced by Helicobacter pylori alter somatostatin release from cultured rabbit fundic D-cells?
N alpha-Methylhistamine had no direct inhibitory effects on D-cells, but TNF-alpha both significantly reduced the cellular content and inhibited release. Inflammatory cytokines, rather than N alpha-methylhistamine, are therefore likely to be responsible for directly inhibiting D-cell function in H pylori infection.
These findings suggest that an extracellular proteolytic pathway in the retina contributes to RGC death via NO-activated MMP-9.