Fig 7. Proposed model.

LPS or bacterial infection interrupted the normal TCA cycle that causes the kinetic expression of succinate and inosine, which corresponds the kinetic expression of il1b/IL1β and c3/C3, respectively, representing a metabolic regulation of the transition from cellular innate immunity to hurmoral immunity. Succinate inhibits the enzymatic activity of PHD that promotes the degradation of HIF-1α at the phase of cellular innate immunity. But inosine competitively bind to PHD to rescue the activity of PHD at the phase of humoral innate immunity to promote the occurrence of humoral innate immunity.