Abstract

Experimental in vivo infection models have been widely proven as an effective tool for the investigation of pathogen-specific host immune responses during bovine mastitis. Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) are two common mastitis pathogens with an opposite clinical outcome of the disease. E. coli and S. aureus have proven to be valid surrogates to model clinical and subclinical mastitis respectively. Transcriptome profiling studies demonstrated that the transcriptional response in the teat reflects the course of pathogen-specific mastitis, being ultimately determined by the immune response of the mammary epithelial cells. After experimental in vivo challenge, E. coli induces a vigorous early transcriptional response in udder tissue being quantitatively and qualitatively distinct from the much weaker response against an S. aureus intramammary infection. E. coli mastitis models proved that the local response in the infected udder quarters is accompanied by a response in non-infected neighbouring udder quarters modulating systemically their immune responsiveness. This insight resulted in the approach to prime tissue resident cells with pathogen-derived molecules to achieve temporary protection of the udder in increasing the expression of endogenous antimicrobial peptides and lowering of the severity of an eventually occurring inflammatory response.