|Ryman, V - Michigan State University|
|Pighetti, G - University Of Tennessee|
|Gandy, J - Michigan State University|
|Applegate, C - Michigan State University|
|Sordillo, L - Michigan State University|
Submitted to: Prostaglandins & Other Lipid Mediators
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/8/2015
Publication Date: 9/30/2015
Citation: Ryman, V.E., Pighetti, G.M., Lippolis, J.D., Gandy, J.C., Applegate, C.M., Sordillo, L.M. 2015. Quantification of bovine oxylipids during intramammary Streptococcus uberis infection. Prostaglandins & Other Lipid Mediators. doi: 10.1016/j.prostaglandins.2015.09.006.
Interpretive Summary: Streptococcus uberis mastitis results in severe mammary tissue damage in dairy cows due to uncontrolled inflammation. Specific types of lipids are potent immune mediators that modulate pathogen-induced inflammatory responses. This work determines how lipid based immune mediators change concentration in milk and mammary tissues during different stages of S. uberis mastitis. We found that specific lipids were significantly increased in S. uberis-infected bovine mammary tissue. These findings identify specific lipids that may contribute some of the dynamics of inflammation during bacterial infection.
Technical Abstract: 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.