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ARS Home » Research » Publications at this Location » Publication #191291


item Bannerman, Douglas
item Paape, Max

Submitted to: Veterinary Immunology and Immunopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/29/2006
Publication Date: 8/15/2006
Citation: Bannerman, D.D., Paape, M.J., Chockalingam, A. 2006. Staphylococcus aureus intramammary infection elicits increased production of transforming growth factor-alpha beta1, and beta2. Veterinary Immunology and Immunopathology. 112(304):309-315.

Interpretive Summary: Staphylococcus aureus remains one of the most prevalent contagious mastitis pathogens. The ability of S. aureus to establish infection is due, in part, to the ability of the host to mount an immune/inflammatory response to the bacteria. Increased knowledge of mammary gland innate immune responses has the potential to lead to the development of immuno-modulatory interventions that can be used in the treatment of mastitis. The current study is the first to investigate changes in TGF-a, TGF-b1, and TGF-b2 during the course of intramammary infection with S. aureus. Although a previous study reported on changes in the expression of these cytokines in the context of experimental E. coli mastitis, extrapolation of those findings to S. aureus is difficult due to the distinct cytokine responses elicited by these two pathogens in vivo. This study clearly establishes that S. aureus is able to evoke increased production of TGF-a, TGF-b1, and TGF-b2 during the course of intramammary infection. Further studies will be needed to identify the direct role that these cytokines have on the outcome of intramammary infection caused by this and other mastitis pathogens.

Technical Abstract: Staphylococcus aureus is one of the most highly prevalent contagious pathogens to cause mastitis in cattle. S. aureus is able to evade host defense mechanisms and can persist in the mammary gland throughout the lifetime of the animal. In contrast to the pro-inflammatory response elicited by other mastitis pathogens, the host response to S. aureus is marked by the absence of the induction of critical pro-inflammatory cytokines, including IL-8 and TNF-a. The lack of production of such pro-inflammatory cytokines has been reported to correspond with the ability to establish chronic infection. Although differential induction of IL-8 and TNF-a has been well-characterized in response to S. aureus and other mastitis-causing pathogens, elucidation of changes in the expression of other mediators with the potential to regulate mammary inflammatory responses remains lacking. Transforming growth factor (TGF)-a, TGF-b1, and TGF-b2 are cytokines that have been implicated in regulating mammary gland development and shown to moderate inflammation. All of these cytokines are expressed in the mammary gland and their levels of expression have been shown to change during the course of Escherichia coli intramammary infection. Because these cytokines have a demonstrated role in mediating inflammatory responses and there is known pathogen-dependent differential expression of inflammatory-regulating cytokines, the objective of the current study was to determine whether S. aureus intramammary infection influences TGF-a, TGF-b1, and TGF-b2 concentrations in the mammary gland. Ten mid-lactating Holstein cows were challenged with either phosphate-buffered saline or 67 CFU of S. aureus and milk samples collected. Increases in milk levels of TGF-a were evident within 32 h of infection and persisted for 16 h. Infection with S. aureus also elicited an increase in TGF-b1 and TGF-b2 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-a, S. aureus is able to elicit host production of TGF-a, TGF-b1, and TGF-b2. This finding suggests a role for these molecules in mediating mammary gland host innate immune responses to infection by S. aureus.