Send to

Choose Destination
Vet Res. 2009 Jul-Aug;40(4):31. doi: 10.1051/vetres/2009014. Epub 2009 Mar 27.

Assessment of the immune capacity of mammary epithelial cells: comparison with mammary tissue after challenge with Escherichia coli.

Author information

Research Institute for the Biology of Farm Animals (FBN), Molecular Biology Research Unit, Dummerstorf, Germany.


We examined the repertoire and extent of inflammation dependent gene regulation in a bovine mammary epithelial cell (MEC) model, to better understand the contribution of the MEC in the immune defence of the udder. We challenged primary cultures of MEC from cows with heat inactivated Escherichia coli pathogens and used Affymetrix DNA-microarrays to profile challenge related alterations in their transcriptome. Compared to acute mastitis, the most prominently activated genes comprise those encoding chemokines, interleukins, beta-defensins, serum amyloid A and haptoglobin. Hence, the MEC exert sentinel as well as effector functions of innate immune defence. E. coli stimulated a larger fraction of genes (30%) in the MEC belonging to the functional category Inflammatory Response than we recorded with the same microarrays during acute mastitis in the udder (17%). This observation underscores the exquisite immune capacity of MEC. To more closely examine the adequacy of immunological regulation in MEC, we compared the inflammation dependent regulation of factors contributing to the complement system between the udder versus the MEC. In the MEC we observed only up regulation of several complement factor-encoding genes. Mastitis, in contrast, in the udder strongly down regulates such genes encoding factors contributing to both, the classical pathway of complement activation and the Membrane Attack Complex, while the expression of factors contributing to the alternative pathway may be enhanced. This functionally polarized regulation of the complex complement pathway is not reflected in the MEC models.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for EDP Sciences Icon for PubMed Central
Loading ...
Support Center