The Changes Of T Cell Subsets In Mastitis Caused By Staphylococcus Aureus In Mice

Mastitis is one of the most harmful diseases in the dairy industry of world, which resultsan enormous economic cost and threats food safety. The overuse of antibiotics in clinic causesa serious of problems, such as drug resistance and residues. To resolve these problems,improving immunocompetence resistant to microorganism’s infection is the key point.Because of the deficient of reagents in ruminants, it is acceptable to research mastitis inmouse.In order to understand the immune responses in the mastitis and provide theoretical basisfor vaccine development, we established the mastitis in mouse with the isolatedStaphylococcus aureus (S. aureus) from subclinical mastitis in dairy goats. And the T cellsubsets participated in the immune responses to S. aureus in the mammary gland and spleenwere detected with Flow cytometry.Using1×108CFU/ml staphylococcus aureus to infect mouse’s mammary gland, after theinfection stopping breast-feeding, succeefully induced the mouse having acute mastitis. Theclinical condition appears as, depressed, rare drive inconvenient, abdomen inflamed. Anatomyshows that mammary gland with severe bleeding, peritoneum having large amount infectiveexudate. Bacteria counting show bacteria grow really fast, and reach the maximum after24hours. Tissue slice can observe large amount infection cells, mammary tissue iscomparatively complete.The results as following:1.The acute mastitis was successfully established in mouse, which was infused with1×108CFU/ml S. aureus in the mammary gland and not breastfeed. The obvious clinicalsymptoms were observed in mouse, including acting depressed, stiff of hind legs, redness andswelling of the abdomen. Serious bleeding and plenty of inflammatory exudates wereobserved in the mammary gland and peritoneum, respectively. The bacteria growth and thepeak at24h post infection were determined with bacteria counting method. From tissuebiopsies, a great deal of inflammatory cells was infiltrated in the mammary gland, and breasttissue was observed completely. 2.The chronic mastitis was successfully established in mouse by using4×107CFU/ml S.aureus infection in the mammary gland, which normally nurses the offspring post infection12h. No clinical symptoms were observed on the abdomen. Patho-anatomy revealed that pustulewas observed in the mammary gland post infection2-3d. The bacterial counting had begun topeak off post infection5d. From tissue biopsies, the structure of breast tissue was destroyedand acinar epithelial arranged disorderly. Inflammatory cells infiltration and ducts and aciniepithelial hyperplasia were both found in the mammary gland.3.In innate immunity, the significant increase of IL-17+γδ T cells was consistent with thechange of bacterial counting in the mammary gland by Flow cytometry. In adaptive immunity,Th1, Th2, Th17, Treg and CD8+T cells were significantly increased post infection5d, whichwas also consistent with the change of bacterial number. However, only Th2and CD8+T cellswere significantly increased in spleen.In conclusion, IL-17+γδ T cells mediate innate immunity against S. aureus during earlystage of mastitis. All of Th, Treg and CD8+T cells were participated in the adaptive immunityagainst S. aureus infection. Th2and CD8+T cells were orchestrated peripheral immuneresponse in mastitis.