Influence Of The Exogenous IL-6 And TNF-α On Apoptosis Of Milk Neutrophil Cell In Bovine Mastitis

Objective:To better understand the role of IL-6, TNF-a for neutrophil cells apoptosis in milk with bovine mastitis, milk neutrophil cells with bovine mastitis were exposed to exogenous IL-6、TNF-a and the mixture of TNF-a and IL-6. This information will provide experimental evidence for further research on pathogenesis ofmastitis in dairy cows.Method:The neutrophil isolated from milk suffering from mastitis were exposed to different concentrations ofexogenous IL-6、TNF-a or the mixture of TNF-a and IL-6. The neutrophil cells were stained or used flow cytometry to indenify the role of TNF-a and IL-6 in neutrophil apotosis at different time.Result:(1) The somatic cells isoated from cow milk were neutrophils with bovine peripheral blood neutrophil cell isolation liquid separation (2) 0.05ng/mL、0.1ng/mL、 0.2ng/mL、0.5ng/mL ectogenic IL-6 had an inhibitory effect on milk neutrophil cell in bovine Mastitis for 6-72 h. (3) 2ng/mL、5ng/mL、10ng/mL、20ng/mL ectogenic TNF-a promote milk neutrophil apoptosis between 6 h and 48 h. (4) Ectogenic IL-6 and TNF-a of 1:100 and 1:50 proportion promoted milk neutrophil cell apoptosis in bovine mastitis; 100:1 and 50:1 proportion have an inhibitorye effect on milk neutrophil apoptosis between 6 h and 48 h and 1:1 proportion promoted milk neutrophil apoptosis excepte for 12 h.Conclusion:The somatic cells isoated from cow milk were neutrophils with bovine peripheral blood neutrophil cell isolation liquid separation. Ectogenic IL-6 have an inhibitory effect on milk neutrophil cell in bovine mastitis. Ectogenic IL-6 have an inhibitory effect on milk neutrophil cell in bovine mastitis. Ectogenic TNF-a have an contribute effect on milk neutrophil apoptosis between 6 and 48 hours.The neutrophil was exposed to different concentration of ectogenic IL-6 and TNF-a, IL-6 inhibited the neutrophil apotosis, and TNF-a promoted neutrophil apoptosis,. However, TNF-a had a stronger effect on promoting neutrophil apoptosis than inhibition of IL-6.