In the early stage of infection, the body may accelerated the degradation of TSG-6 through the activation of specific proteases, resulting in significantly lower TSG-6 levels in the model group and the treatment group compared with the control group, while the treatment group obtained exogenous TSG-6 supplemented from dams during the fetal period, which could temporarily restore the anti-inflammatory efficacy of the period, and thus the TSG-6 levels in the treatment group were higher than those in the model group. This evidence concerns the gene TNFAIP6 and infection.