We demonstrate that genetic, pharmacological, and hypoxia-mediated Hif-1α stabilization upregulated macrophage tnfa. We utilize well-characterized, non-invasive, zebrafish models of inflammation and infection to show that Hif-1α-mediated tnfa acts via an alternative, cyclooxygenase dependent mechanism, that differs from better understood DAMP/PAMP mediated pathways that are cyclooxygenase independent (15, 16). This evidence concerns the gene HIF1A and infection.