Bovine mammary immune response to an experimental intramammary infection with a Staphylococcus aureus strain containing a gene for staphylococcal enterotoxin C1

Staphylococcal enterotoxin C (SEC), a superantigen, is the most frequently expressed enterotoxin by bovine strains of Staphylococcus aureus causing ma stitis. To examine the possible impact of SEC on the immune response of the bovine mammary gland, we monitored changes in lymphocyte subpopulations in mammary glands of four lactating cows after intramammary instillation of S . aureus strain Rn4220 transformed with a plasmid containing a gene coding for SEC1 Four other lactating cows received the same strain transformed wit h the plasmid without the SEC1 gene (positive control), and four cows were untreated (negative control). Mammary quarter milk samples for somatic cell count (SCC) analysis and determination of N-acetyl-beta -D-glucosimindase (NAGase) activity levels were collected daily for 21 d postinstillation. Fl ow cytometry utilizing three-color analysis was used to phenotype lymphocyt e subpopulations isolated from milk samples collected on d 0, 4, 7, 11, 14, 18, and 21 postinstillation from all the cows. Milk from mammary gland hal ves (positive control and experimental) or all mammary quarters (negative c ontrol) was collected for flow cytometric analysis. Increased NAGase activi ty, SCC, and isolated S. aureus demonstrated that infection was established in mammary quarters intrammarily instilled with bacteria. There were no si gnificant differences (P > 0.05) in the proportions of BoCD4 helper T lymph ocytes or BoCD8 cytotoxic T lymphocytes between the two infected treatment groups. There was a significant day x treatment difference of the proportio n of a gamma delta T cell subpopulation that did not express BoCD2, but did express the ACT2 activation molecule and a significant treatment differenc e of a gamma delta T cell subpopulation that expressed BoCD2, but not the A CT2 activation molecule (P < 0.05). Results do not support the hypothesis t hat the presence of the gene for SEC1 alters the mammary BoCD4 or BoCD8 T l ymphocyte response to infection.