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Title: STAPHYLOCOCCUS AUREUS INTRAMAMMARY INFECTION ELICITS INCREASED PRODUCTION OF TRANSFORMING GROWTH FATOR-ALPHA, BETA1, AND BETA2.

Author
item Bannerman, Douglas
item Paape, Max
item CHOCKALINGAM, ANNAPOORANI - PENN STATE UNIVERSITY

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 6/5/2006
Publication Date: 9/4/2006
Citation: Bannerman, D.D., Paape, M.J., Chockalingam, A. 2006. Staphylococcus aureus intramammary infection elicits increased production of transforming growth fator-alpha, beta1, and beta2. [abstract]. IN: 2nd European Veterinary Immunology Workshop Program and Book of Abstracts. p. 15, Sept. 4-6, 2006, Paris, France.

Interpretive Summary:

Technical Abstract: Staphylococcus aureus is one of the most highly prevalent contagious pathogens to cause mastitis in cattle. In contrast to other mastitis pathogens, the host response evoked during S. aureus intramammary infection is marked by the absence of the induction of critical cytokines, including IL-8 and TNF-alpha, which have established roles in mediating host innate immunity. The elucidation of changes in the expression of other mediators with the potential to regulate mammary inflammatory responses to S. aureus remains lacking. Transforming growth factor (TGF)-alpha, TGF-beta1, and TGF-beta2 are cytokines that regulate mammary gland development. Because these cytokines also have a demonstrated role in mediating inflammation, the objective of the current study was to determine whether S. aureus intramammary infection influences their expression. Ten cows were challenged with S. aureus and milk samples collected. Increases in milk levels of TGF-alpha were evident within 32 h of infection and persisted for 16 h. Infection with S. aureus also elicited an increase in TGF-beta1 and TGF-beta2 production within 40 h of infection and this increase was sustained through the end of the study 5 days later. Thus, in contrast to IL-8 and TNF-alpha, S. aureus is able to elicit host production of TGF-alpha, TGF-beta1, and TGF-beta2. This finding may suggest a role for these molecules in mediating mammary gland host innate immune responses to infection by S. aureus.