Staphylococcus aureus intramammary infection elicits increased production of transforming growth factor-α, β1, and β2

In contrast to other mastitis pathogens, the host response evoked during Staphylococcus aureus intramammary infection is marked by the absence of the induction of critical cytokines, including IL-8 and TNF-α, 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)-α, TGF-β1, and TGF-β2 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-α were evident within 32 h of infection and persisted for 16 h. Increases in TGF-β1 and TGF-β2 levels were detected within 40 h of S. aureus infection and persisted through the end of the study. Thus, in contrast to IL-8 and TNF-α, S. aureus elicits host production of TGF-α, TGF-β1, and TGF-β2. This finding may suggest a role for these cytokines in mediating mammary gland host innate immune responses to S. aureus.