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Title: The pathogen-dependent variations in the innate immune response to intramammary infection

Author
item Bannerman, Douglas

Submitted to: Joint Abstracts of the American Dairy Science and Society of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: 3/20/2008
Publication Date: 7/11/2008
Citation: Bannerman, D.D. 2008. The pathogen-dependent variations in the innate immune response to intramammary infection. Joint Abstracts of the American Dairy Science and Society of Animal Science. Abstract. No. 811.

Interpretive Summary:

Technical Abstract: Mastitis remains one of the most prevalent diseases among dairy cows and one of the most economically costly diseases to the dairy industry. The majority of cases of mastitis result from intramammary bacterial infection, and numerous genera of bacteria are capable of inducing mastitis. Following penetration of the physical barriers of the teat canal, the innate immune system encompasses the initial and primary mechanism by which the cow defends itself against invading bacterial pathogens. It has been well-described that some pathogens are readily eliminated from the mammary gland, and the accompanying mastitis quickly resolved. In other cases, bacterial pathogens can persist in the gland resulting in chronic mastitis that may endure throughout the lifespan of the cow. During the past few years, there have been rapid gains in the knowledge surrounding the innate immune responses that are evoked in response to intramammary infection. A major finding from this area of research is that despite the highly conserved nature of the elements involved in host innate immunity, marked variation in innate immune responses to different bacterial pathogens can occur. This review summarizes evidence that the nature of the innate immune response, as well as the rapidity in which it is evoked, influences the outcome of intramammary infection. Furthermore, the utility that immune response modifiers may have in preventing and/or treating mastitis will be considered.