Effects Of NF-κB Signal Pathway And Cytokine In Staphylococci Aureus Panton Valentine-leukocidin Associated Pneumonia

Objective: The purpose of this experiment was to study the lesions characteristicof acute lung injury in mice which was caused by Staphylococcus aureusPanton-Valentine leukocidin (PVL). The effects of nuclear transcription factor-κB(NF-κB) signaling pathway proteins and cytokines in lung injuryMethods：60Balb/c mice were distributed into four groups in random, group．Theywere A group(infected with rPVL)，B(infected withPVL-positive stains culture supernatant),C(with PVL-nagative stains culturesupernatant)，D(contral group，with saline).All the mice were infected by endotrachealintubation. After infected, WBCs in peripheral bloodstream were collected forcounted.The lung was removed from the mice for histological observations. Exfoliatedcells of BALF were collected, apoptosis and necrosis rates of PMNs were analyze.ELISA was performed to evaluate levels of TNF-α、IL-8、IL-10、MCP-1.At the3h and9h, NF-κB of the lung tisure were respectively detected with RT-PCR andimmunohistochemical SABC method.Results: Compared with the D group, mice in A,Bgroups showed symptoms ofsevere illness：lethargy,diffuse infiltration of inflammatory cells, hemorrhage, edemaand other manifestations of lung injury. The leukocyte and neutrophil count inperipheral blood were decreased,the rate of neutrophil apoptosis and necrosis in BALFwere increased. The expression of NF-κBmRNA and NF-κB p65protein in Lunghomogenate were increased gradually with the action time. TNF-α, IL-8, IL-10increased gradually.Mice in C group has no significant changes in lung.Conclusions: PVL can cause hemorrhagic inflammatory in mice. NF-κB signalingpathway activation and cytokine release play an important role in PVL-related lunginjury.