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Brief Overview of mammary gland immunity

Mammary gland immunity is defined as the ability of the gland to resist and recover from infectious disease and is accomplished by both innate and specific immunity. Innate immunity is either non-specific or bacterial pathogen specific and is the principal immunity in the uninfected udder and in the early stages of disease.  In the majority of cases, the innate system functions rapidly and infection is eliminated often without any noticeable signs of disease.  The physical structure of the teat end, biochemical properties of keratin, macrophages, neutrophils and some soluble factors such as lactoferrin (in the dry period) are all components of the innate system. Recent studies have shown that macrophages have bacteria specific receptors (toll-like receptors) that recognize components of bacteria. An example of this is the toll-like–4 receptor (TLR4) that recognizes LPS in gram-negative bacteria such as E. coli and Klebsiella species.

Specific or acquired immunity is triggered if the non-specific system is unsuccessful at eliminating the pathogen, or if the infecting agent has been encountered in a previous infection episode.  This response is elicited by antigen combining with specific proteins of  Major Histocompatability Complex (MHC) molecules and is mediated by macrophages, lymphocytes and immunoglobulins.

Normal milk contains a variety of cells: polymorphonuclear, lymphocytes, eosinophils, macrophages and epithelial cells. In milk from non-infected cows, macrophages are the dominant type and constitute 30-75% of the cell population.  Upon encountering pathogens, macrophages phagocytose them and destroy them with proteases and reactive oxygen species then secrete cytokines that act as chemoattracts (for example complement5a, interleukin-1 [IL-1], and TNF- α) that stimulate rapid influx of PMNs from the peripheral circulation into the mammary gland. The speed and number of PMNs influx into the mammary gland and their ability to effectively phagocytose and kill bacteria controls the outcome of intramammary infection and the severity of disease.

Tumor necrosis factor-α (TNF- α) is one of the cytokines involved in the acute, systemic inflammatory response to a coliform intramammary infection. In extreme cases such cytokines may produce an uninhibited inflammatory response that can result in an endotoxic shock.  Secretion of this cytokine is in response to macrophage stimulation and is higher in periparturient cows than in cows in late lactation.  Such cytokine responses (called cytokine profiles) are bacteria specific. For example the TNF- α production is virtually absent in cows challenged with Staphylococcus aureus.

Opsonization (binding of antibody to a receptor on the pathogen’s cell wall) increases the phagocytosis of bacteria by PMN’s.   IgG2 and IgM are the primary antibodies responsible for opsonization.  Some research has shown that the level of IgG is lower in cows around calving and may partially account for the increased incidence of mastitis early in lactation.

Stressors around parturition may also have a dramatic effect on the function of PMN’s and can result in reduced random migration and oxidative metabolism. Several studies have shown that a severe negative energy balance as evaluated by an increase in Non-Esterified Fatty Acids (NEFA’s) and or β-hydroxybutyrate leads to a poor response of PMSs. Similarly, high levels of growth hormone and cortisol are associated with reduced competence of PMN’s.