Staphylococcus aureus and Escherichia coli are among the most prevalent species of gram-positive and gram-negative bacteria, respectively, that induce clinical mastitis. The innate immune system comprises the immediate host defense mechanisms to protect against infection and contributes to the initial detection of and proinflammatory response to infectious pathogens. The objective of the present study was to characterize the different innate immune responses to experimental intramammary infection with E. coli and S. aureus during clinical mastitis. The cytokine response and changes in the levels of soluble CD14 (sCD14) and lipopolysaccharide-binding protein (LBP), two proteins that contribute to host recognition of bacterial cell wall products, were studied. Intramammary infection with either E. coli or S. aureus elicited systemic changes, including decreased milk output, a febrile response, and induction of the acute-phase synthesis of LBP. Infection with either bacterium resulted in increased levels of interleukin 1 (IL-1), gamma interferon, IL-12, sCD14, and LBP in milk. High levels of the complement cleavage product C5a and the anti-inflammatory cytokine IL-10 were detected at several time points following E. coli infection, whereas S. aureus infection elicited a slight but detectable increase in these mediators at a single time point. Increases in IL-8 and tumor necrosis factor alpha were observed only in quarters infected with E. coli. Together, these data demonstrate the variability of the host innate immune response to E. coli and S. aureus and suggest that the limited cytokine response to S. aureus may contribute to the well-known ability of the bacterium to establish chronic intramammary infection.
This investigation evaluated mammary cell loss and replacement during lactation and the impact of administration of bST on these processes. During lactation, a gradual decrease in number of mammary epithelial cells within the mammary glands occurs and largely accounts for the decline in milk production with advancing lactation. This decrease is not appreciably impacted by the loss of viable epithelial cells in milk. Rather, the net decline in cell number (approximately 50% during the entire lactation) results from continual death by apoptosis. Accompanying the decline in mammary cell number by apoptosis is a degree of cell renewal. Approximately 0.3% of mammary cells in lactating, nonpregnant cows were labeled by a 24-h in vivo treatment with the thymidine analog, bromodeoxyuridine. During the entire lactation, the number of new cells amounts to approximately 50% of the number of cells initially present. By the end of lactation, most cells present in the mammary gland were formed after calving. Increasing cell replacement or decreasing apoptosis during lactation may provide a means to increase persistency of lactation. Indeed, administration of bST to Holstein cows during midlactation increased the proportion of mammary epithelial cells expressing the nuclear proliferation antigen, Ki-67, from 0.5 to 1.6%. Bovine somatotropin appears to increase the rate of cell renewal in the lactating mammary gland. Knowledge of molecular regulation of apoptosis and cell proliferation should provide a means to modulate cell turnover in the mammary gland. A change in the ratio of epithelial proliferation to cell death during lactation will affect the persistency of lactation.
A persistent lactation is dependent on maintaining the number and activity of milk secreting cells with advancing lactation. When dairy cows are milked twice daily, the increase in milk yield from parturition to peak lactation is due to increased secretory activity per cell rather than to accretion of additional epithelial cells. After peak lactation, declining milk yield is due to loss of mammary epithelial cells by apoptosis. During lactation, only 0.3% of mammary cells proliferate in a 24-h period. Yet this proliferative rate is sufficient to replace most mammary epithelial cells by the end of lactation. Management practices can influence lactation persistency. Administration of bovine somatotropin may enhance persistency by increasing cell proliferation and turnover, or by reducing the rate of apoptosis. Increased photoperiod may also increase persistency of lactation by mechanisms that are as yet undefined. Increased milking frequency during the first weeks of lactation increases milk yield, even after return to less frequent milking, with increases of approximately 8% over the entire lactation. A mammary cell proliferation response to frequent milking during early lactation appears to be involved. Conversely, advanced pregnancy, infrequent milking, and mastitis increase death of epithelial cells by apoptosis. Regulation of mammary cell renewal provides a key to increasing persistency. Investigations to characterize epithelial cells that serve as the proliferative population in the bovine mammary gland have been initiated. Epithelial cells that stain lightly in histological sections are evident through all phases of mammary development and secretion and account for nearly all proliferation in the prepubertal gland. Characterization of these cells may provide a means to regulate mammary cell proliferation and thus to enhance persistency, reduce the effects of mastitis, and decrease the necessity for a dry period.
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