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Background  Information generated via microarrays might uncover interactions between the mammary gland and  Streptococcus uberis  (  S. uberis  ) that could help identify control measures for the prevention and spread of  S. uberis  mastitis, as well as improve overall animal health and welfare, and decrease economic losses to dairy farmers. The main objective of this study was to determine the most affected gene networks and pathways in mammary tissue in response to an intramammary infection ( IMI ) with  S. uberis  and relate these with other physiological measurements associated with immune and/or metabolic responses to mastitis challenge with  S. uberis  O140J.    Results   Streptococcus uberis  IMI resulted in 2,102 (1,939 annotated) differentially expressed genes ( DEG ). Within this set of DEG, we uncovered 20 significantly enriched canonical pathways (with 20 to 61 genes each), the majority of which were signaling pathways. Among the most inhibited were  LXR/RXR Signaling  and  PPARα/RXRα Signaling . Pathways activated by IMI were  IL-10 Signaling  and  IL-6 Signaling  which likely reflected counter mechanisms of mammary tissue to respond to infection. Of the 2,102 DEG, 1,082 were up-regulated during IMI and were primarily involved with the immune response, e.g.,  IL6 ,  TNF ,  IL8, IL10, SELL, LYZ , and  SAA3 . Genes down-regulated (1,020) included those associated with milk fat synthesis, e.g.,  LPIN1, LPL, CD36 , and  BTN1A1 . Network analysis of DEG indicated that  TNF  had positive relationships with genes involved with immune system function (e.g.,  CD14, IL8, IL1B , and  TLR2 ) and negative relationships with genes involved with lipid metabolism (e.g.,  GPAM ,  SCD ,  FABP4 ,  CD36 , and  LPL ) and antioxidant activity ( SOD1 ).    Conclusion  Results provided novel information into the early signaling and metabolic pathways in mammary tissue that are associated with the innate immune response to  S. uberis  infection. Our study indicated that IMI challenge with  S. uberis  (strain O140J) elicited a strong transcriptomic response, leading to potent activation of pro-inflammatory pathways that were associated with a marked inhibition of lipid synthesis, stress-activated kinase signaling cascades, and PPAR signaling (most likely PPARγ). This latter effect may provide a mechanistic explanation for the inverse relationship between immune response and milk fat synthesis.

bmc genomics

Gene network and pathway analysis of bovine mammary tissue challenged with Streptococcus uberis reveals induction of cell proliferation and inhibition of PPARγ signaling as potential mechanism for the negative relationships between immune response and lipid metabolism