The glucocorticoid inhibits neutrophils formed extracellular traps (NETs) and suppresses the inflammation caused by fallopian tube staphylococcal infection

S.-X. Luan, X.-H. Chen

Department of Reproductive Medicine, Weifang People’s Hospital, Weifang, Shandong, China. zhenyunyin123@sina.com

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• Pharmacology

OBJECTIVE: Fallopian tube can transport zygote into the uterine cavity, while inflammation may cause certain influences on the fallopian tube’s function. Neutrophils formed extracellular traps (NET) can kill pathogenic microorganisms. This study intends to analyze the role of glucocorticoid in the regulation of NETs sterilization during the fallopian tube staphylococcal infection.

MATERIALS AND METHODS: Rat fallopian tube staphylococcal infection model was established. Group A was the control group, group B was the model group, and group C was the dexamethasone intervention group. ELISA was applied to test inflammatory factors, including citrullinated histone H3 (CitH3) and high molecular weight kininogen (HK) content in serum. RT-PCR was performed to test the mRNA expression of glucocorticoid receptor α, β (GR-α, GR-β). Western blot was used to detect the protein levels of GR-α and GR-β.

RESULTS: Microscopically, group A showed clear fallopian tube wall and unobstructed lumen. Group B presented obscured tube wall, blocked lumen, and inflammatory cells infiltration. Group C demonstrated unclear tube wall and a few inflammatory cells infiltration. Serum CitH3 level was increased, while HK was down-regulated in group B compared with group A. CitH3 was declined, whereas HK was enhanced in group C compared with group B (p<0.05). The mRNA expression of GR-β was reduced, while GR-α expression was elevated in group C compared with group A and B. Group B showed upregulated GR-β expression and reduced GR-α mRNA and protein expression compared with group A (p<0.05).

CONCLUSIONS: Rat fallopian tube Staphylococcus aureus infection activates NETs, elevates CitH3, and decreases HK. Glucocorticoid can inhibit inflammation through down-regulate GR-β and up-regulate GR-α expression.

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