13-hydroperoxylinoleic-acid and Mastitis--Bovine

Streptococcus uberis mastitis results in severe mammary tissue damage in dairy cows due to uncontrolled inflammation. Oxylipids are potent lipid mediators that orchestrate pathogen-induced inflammatory responses, however, changes in oxylipid biosynthesis during S. uberis mastitis are unknown. Thus, the current objective was to determine how oxylipid concentrations change in milk and mammary tissues during different stages of S. uberis mastitis. Increased arachidonic acid and linoleic acid-derived oxylipids were significantly increased in S. uberis-infected bovine mammary tissue. Linoleic acid metabolites, hydroxyoctadecadienoic acid (HODE) and oxooctadecadienoic acid, predominated in tissue and milk. Furthermore, in vitro exposure of bovine mammary endothelial cells to 13-hydroperoxyoctadecadienoic acid, upstream metabolite of HODE, significantly increased cyclooxygenase-2 expression, but 13-HODE exposure had no effect. The findings in the current study indicate lipidomic profiling may explain some of the dynamics of inflammation during bacterial challenge, however continued research is necessary to determine sample compartments which best reflect disease pathogenesis.

Topics: Animals; Animals, Inbred Strains; Cattle; Cell Adhesion Molecules; Cells, Cultured; Cyclooxygenase 2; Cytokines; Dairying; Eicosanoids; Endothelium, Vascular; Female; Host-Pathogen Interactions; Linoleic Acids; Mammary Glands, Animal; Mastitis, Bovine; Milk; RNA, Messenger; Streptococcal Infections; Streptococcus; Up-Regulation