Objective  To investigate the pneumonic injury features of zinc finger protein A20 mutant (A20△) transgenic mice with experimental sepsis

and approach the regulation roles of A20△ and underlying mechanism.   Methods  Totally 72 Kunming mice were randomly divided into 3 groups

control

LPS group and A20△ transgene group. The mice of the control group received an injection of 1.6 ml normal saline through tail vein

those from the LPS group underwent an injection of 1.6 ml normal saline and then 2.5 mg/kg LPS in 8 h later

while those in A20△ transgene group were injected with 10 μg/1.6 ml plasmid pCAGGS-A20△ followed by an injection of 2.5 mg/kg LPS in 8 h after the first injection. The mice were killed in 3

6

12 and 24 h after LPS injection and their lungs were resected. The quantity of mononuclear macrophage infiltrating in the lung was detected by flow cytometry. The levels of A20 mutant

TNF-α and IL-1β were analyzed by ELISA. The lung-body index and pathologic examination were recruited to accredit lung injury.   Results  In A20△ transgene group

the lungbody indexes were decreased obviously than that of LPS Group in 6

12 and 24 h after LPS injection (P0.05

0.01). The amount of mononuclear macrophage infiltrating in the lung were decreased obviously than that of LPS group (P0.01). In 3 and 6 h after injection LPS

the levels of TNF-α in pneumonic tissue were decreased obviously than that of LPS group (P0.01). The levels of IL-1β in pneumonic tissue were also decreased obviously than that of LPS group (P0.05

0.01). After injection of LPS for 12 and 24 h

there were no difference in the levels of TNF-α and IL-1β in A20△ transgene group and LPS group (P0.05). The results of pathologic examination indicated that the pneumonic injury of A20△ transgene group was milder than LPS Group.   Conclusion  A20△ transgenic mice withstands the pneumonic inflammatory damages in LPS-induced sepsis at some extent

and the mechanism may be through suppressing the infiltration of monocytes to pneumonic tissue as well as decreasing the levels of inflammatory cytokines.