Effect of Streptococcus uberis on Gamma Delta T Cell Phenotype in Bovine Mammary Gland

In this study, we focused analyzing γδ T cells during bovine mammary gland inflammation induced by Streptococcus uberis. A mammary gland cell suspension was obtained using lavage 24, 48, 72, and 168 h after intramammary-induced infection. The proportion of lymphocytes increased during the entire week in which inflammation was present. The γδ T cells were also elevated during inflammation, reaching their peak at 72 h following induced inflammation. The percentage of apoptotic lymphocytes continually increased, with the highest proportion occurring 168 h after S. uberis infection. The results show that γδ T cells may be involved in the resolution of inflammation in bovine mammary glands, with the apoptosis of those cells potentially playing an important role.

Abundance of solute carrier family 27 member 6 (SLC27A6) in the bovine mammary gland alters fatty acid metabolism

The Milk FA and transcriptome of bovine mammary tissue indicated that LCFA transport into mammary cells during late lactation. In vitro test underscored how FA transport via SLC27A6 could dictate the utilization of FA for TG synthesis versus oxidation.

Effect of Lipopolysaccharide and Muramyl Dipeptide on Apoptosis of Bovine Mammary Gland Lymphocytes

The aim of this study was to evaluate whether apoptosis of lymphocytes is modulated by stimulation by lipopolysaccharide (LPS) of Escherichia coli or muramyl dipeptide (MDP). Cell populations were obtained by lavaging of the mammary glands 24, 48, 72, and 168 h following intramammary induced inflammation. The portion of apoptotic lymphocytes peaked at 48 h after treatment with LPS or MDP. The analysis of CD44 expression of the same cell populations showed a higher percentage of CD44-positive lymphocytes 24- and 48-h following induction of inflammation by LPS or MDP. The results demonstrate that during both experimental infection of bovine mammary glands with LPS or MDP, apoptosis of lymphocytes was induced in the initial phase of the inflammatory response and CD44 was also overexpressed at the beginning of inflammation. These data suggest a connection of lymphocyte apoptosis with the expression of CD44 receptors.