TRIENNIAL LACTATION SYMPOSIUM/BOLFA: Pathogen-specific immune response and changes in the blood-milk barrier of the bovine mammary gland.

Because of the decreasing use of antimicrobial drugs in animal food production, new treatments of infectious diseases such as mastitis are needed. This includes strategies to optimize the function of the animal's immune system. The present review discusses the components of the mammary immune response and the involvement of the blood-milk barrier during infections with different bacteria, strategies to manipulate the blood-milk barrier, and the potential to increase the efficiency of the animal's immune response. The mammary immune response is widely based on the cellular components of the innate immune system, which can be detected as an increase of the somatic cell count (SCC). During infection with Gram-negative bacteria such as , characterized by severe clinical symptoms, there is a considerable transfer of soluble blood components including immunoglobulins from blood into milk. This is not typically observed during intramammary infection with Gram-positive bacteria such as , which is typically observed as a chronic subclinical infection. We have simulated these different types of mastitis by administering cell wall components of these bacteria (i.e., lipopolysaccharide [LPS] from and lipoteichoic acid [LTA] from ). Dosages of these 2 components intramammarily administered were adjusted to induce a comparable increase in SCC. Treatment with LPS caused a comprehensive transfer of blood components including immunoglobulins into milk, whereas in the LTA-induced mastitis, only a small increase of blood components in milk occurred. The blood-milk barrier can be manipulated. Glucocorticoids such as prednisolone reduced the transfer of blood components from blood into milk while reducing the general inflammatory reaction. It is possible that this treatment also inhibits the transfer of immunoglobulins into milk, likely reducing the efficiency of the immune response. In contrast, an opening of the blood-milk barrier could be achieved by an extremely high dosage of oxytocin (e.g., 100 IU). We assume that the myoepithelial hypercontraction increases the epithelial permeability that allows an increased flux of blood components including immunoglobulins into milk. The potential for manipulating the blood-milk barrier permeability as a treatment for mastitis is possible if specific antibodies against pathogens can be efficiently transported to the infected mammary gland