Graduate Student Literature Review: Systemic mediators of inflammation during mastitis and the search for mechanisms underlying impaired lactation

The negative effect of mastitis on lactation is well established, yet the mechanisms causing reduced milk production in the afflicted dairy cow are not. As one of the major inflammatory diseases in the dairy industry, mastitis has rightly received considerable research interest for decades. However, the focus on distinct, pathologic effects in mastitic glands has largely overlooked systemic effects on noninflamed mammary glands. This is particularly evident in the severe, acute response to the potent inflammatory mediator, lipopolysaccharide (LPS). Whereas secretory cell death, impaired tight junctions, and migration of leukocytes are locally restricted to an inflamed, LPS-challenged gland, changes in milk yield and milk components may be detectable in all mammary glands. Further, these differences extend to the mammary transcriptome. Notably, few transcriptomic studies have been designed to test for effects of systemic mediators of inflammation on gene expression. Relevant changes in the noninflamed mammary gland, identified through biochemical analyses and transcriptional studies, warrant further research. Current evidence suggests proinflammatory cytokines play a role in regulating lactose synthesis, but additional candidates and mechanisms continue to be identified. Ultimately, understanding how systemic mediators of inflammation affect mammary function may lead to the development of interventions that enable more efficient milk production without sacrificing the benefits of inflammation.