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The mammary gland is a highly complex organ with tremendous synthetic and secretory capabilities. Injury to mammary tissue results in an inflammatory response characterized by damaged secretory tissue, reduced milk yield, and alterations in milk composition. Changes in milk composition accompanying mammary gland inflammation have been studied extensively and components such as somatic cells and serum albumin are useful as diagnostic markers of mastitis. The magnitude of decreased synthetic and secretory capabilities of mammary epithelium depends in large part on the severity of the inflammatory response. Decreased mammary secretory cell activity is considered to be the outcome of a complex interaction of both microbial and host-related factors. Adherence, multiplication, and toxin production that favor survival of pathogenic bacteria within the mammary gland and the action of macrophages, chemotactic factors, inflammatory mediators, and neutrophil influx have been associated with impaired cellular synthesis, impaired cellular secretion, cellular degeneration, and cell death. However, the series of events that take place after bacterial invasion are not completely understood. Recent evidence suggests that certain bacterial toxins inhibit mammary epithelial cell proliferation in vitro. In addition, changes in mammary epithelial cell gene expression have been observed in response to mammary gland infection. A more thorough understanding of how inflammation affects mammary secretory epithelial cell synthesis and secretion could lead to methods of minimizing production losses associated with intramammary infection of farm animals.
Published in: Journal of Animal Science
Volume 73, Issue suppl_2, pp. 18-18