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Infection and Immunity, March 2006, p. 1907-1915, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1907-1915.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Genome-Wide Expression Analysis of Lipopolysaccharide-Induced Mastitis in a Mouse Model

Lactation and Mammary Gland Biology Group, Department of Animal Science, University of Vermont, Burlington, Vermont 05405,¹ Department of Biology, University of Vermont, Burlington, Vermont 05405²

Received 1 September 2005/ Returned for modification 28 October 2005/ Accepted 8 December 2005

To better understand the acute host response to Escherichia coli mastitis, we analyzed gene expression patterns of approximately 23,000 transcripts 4 h after an intramammary infusion of lipopolysaccharide (LPS) in a mouse model. A total of 489 genes were significantly affected, of which 391 were induced and 98 were repressed. Gene ontology analysis demonstrated that most of the induced genes were associated with the innate immune response, apoptosis, and cell proliferation. Substantial induction of the chemokines CXCL1, CXCL2, and S100A8; the acute-phase protein SAA3; and the LPS binding protein CD14 were confirmed by Northern blot analysis. A subsequent time course experiment revealed CXCL1 induction prior to that of CD14 and SAA3. Mammary epithelial cell cultures also showed marked expression of these factors in response to LPS. The expression of immune-related genes in mammary epithelial cells indicates the importance of this cell type in initiating the inflammatory responses. Repressed genes include several carbohydrate and fatty acid metabolic enzymes and potassium transporters, which may contribute to milk composition changes during mastitis. Therefore, the overall transcription profile, in conjunction with gene ontology analysis, provides a detailed picture of the molecular mechanisms underlying the complex biological processes that occur during LPS-induced mastitis.

Supplemental material for this article may be found at http://iai.asm.org/.

Editor: V. J. DiRita