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Background  Gene expression profiling studies of mastitis in ruminants have provided key but fragmented knowledge for the understanding of the disease. A systematic combination of different expression profiling studies via meta-analysis techniques has the potential to test the extensibility of conclusions based on single studies. Using the program Pointillist, we performed meta-analysis of transcription-profiling data from six independent studies of infections with mammary gland pathogens, including samples from cattle challenged  in vivo  with  S. aureus ,  E. coli , and  S. uberis , samples from goats challenged  in vivo  with  S. aureus , as well as cattle macrophages and ovine dendritic cells infected  in vitro  with  S. aureus . We combined different time points from those studies, testing different responses to mastitis infection: overall (common signature), early stage, late stage, and cattle-specific.    Results  Ingenuity Pathway Analysis of affected genes showed that the four meta-analysis combinations share biological functions and pathways (e.g. protein ubiquitination and polyamine regulation) which are intrinsic to the general disease response. In the overall response, pathways related to immune response and inflammation, as well as biological functions related to lipid metabolism were altered. This latter observation is consistent with the milk fat content depression commonly observed during mastitis infection. Complementarities between early and late stage responses were found, with a prominence of metabolic and stress signals in the early stage and of the immune response related to the lipid metabolism in the late stage; both mechanisms apparently modulated by few genes, including  XBP1  and  SREBF1 .  The cattle-specific response was characterized by alteration of the immune response and by modification of lipid metabolism. Comparison of  E. coli  and  S. aureus  infections in cattle  in vivo  revealed that affected genes showing opposite regulation had the same altered biological functions and provided evidence that  E. coli  caused a stronger host response.    Conclusions  This meta-analysis approach reinforces previous findings but also reveals several novel themes, including the involvement of genes, biological functions, and pathways that were not identified in individual studies. As such, it provides an interesting proof of principle for future studies combining information from diverse heterogeneous sources.

Strengthening insights into host responses to mastitis infection in ruminants by combining heterogeneous microarray data sources