Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 4/7/1999
Publication Date: 4/7/2004
Citation: Paape, M.J., Oostveldt, K.V., Meyer, E. 2004. Journees Nationales GTV-INRA. France. 5 p.
Interpretive Summary: During immune surveillance of mammary tissue by polymorphonuclear leukocytes (PMN), several functionally important receptors are up-regulated, allowing for a more efficient phagocytosis of invading Gram-positive and Gram-negative mastitis pathogens. In vitro studies revealed that PMN and bacterial toxins produce extensive tissue damage that tresults in a decrease in milk synthesis. Furthermore, damage to epithelia cells by toxins secreted by mastitis during bacteria, staphylococcus aureus contributes to the pathogenicity of this organism. Advances in biotechnology have made available tools, techniques, and products for use in mastitis research. The study of programmed of cell death, or apoptosis, may contribute to an understanding of the impairment of PMN function in cows and its relaton to mastitis. The cloning and expression of CD14 may provide a means of neutralizing LPS and minimize its damaging effect on mammary secretory tissue. Use of bifunctional antibodies for targeted cytotoxicity of mastitis pathogens may prove useful in the treatment and prevention of bovine mastitis.
Technical Abstract: The professional phagocytic cells of the bovine mammary gland are neutrophil polymorphonuclear leukocytes (PMN) and macrophages. In the normal mammary gland macrophages are the predominate cells which act as sentinels to invading mastitis causing pathogens. Once the invaders are detected, macrophages release chemical messengers called chemoattractants that cause the directed migration of PMN into the infection. However, their presence is like a double-edged sword. While the PMN are phagocytosing and destroying the invading pathogens, they inadvertently release chemicals which induce swelling of secretory epithelium cytoplasm, sloughing of secretory cells, and decreased secretory activity. Permanent scaring will result in a loss of milk production. Resident and newly migrated macrophages help reduce the damage to the epithelium by phagocytosing PMN through a process called apoptosis. Specific ligands on the neutrophil surface are required for direct migration and phagocytosis. In response to infection, freshly migrated leukocytes express greater numbers of cell surface receptors for immunoglobulins and complement and are more phagocytic than their counterparts in blood. However, phagocytic activity rapidly decreases with continued exposure to inhibitory factors such as milk fat globules and casein in mammary secretions. Compensatory hypertrophy on non-mastitis quarters partially compensates for lost milk production in diseased quarters. Advances in molecular biology are making available tools, techniques, and products to study host-parasite interactions. Successful formation of bifunctional monoclonal antibodies for the targeted lysis of mastitis causing bacteria represents a new line of therapeutics for the control of mastitis in dairy cows.