IL1B and infection: Increased glycolysis and the accompanying breakpoint in the tricarboxylic acid (TCA) cycle at succinate dehydrogenase result in succinate accumulation, which in turn stabilizes the transcription factor hypoxia-inducible factor-1α (HIF-1α) and increases interleukin-1β (IL-1β) expression, linking the metabolic and immune responses to infection [7] (Figure 1A).