The idea is reinforced by the findings that the abundance of SAA1 was significantly increased in gestational tissues in parturition with or without infection, and upon stimulation by bacterial products, pro-inflammatory cytokines and stress hormone glucocorticoids (40, 41, 132), and in turn, SAA stimulated the production of pro-inflammatory mediators including SAA per se, tissue remodeling proteases MMPs as well as prostaglandins PGE2 and PGF2α, the common mediators of labor onset, in gestational tissues (40, 41, 100, 132, 138, 139). Here, SAA1 is linked to infection.