Endometrial epithelial cells play a critical role in mediating inflammatory mechanisms key to
bacterial clearance and tissue re-modelling postpartum. This study characterised innate immune
gene expression by bovine endometrial epithelial cells from three animals in response to
Escherichia coli, a common cause of bovine uterine disease. Expression of key innate immune
genes, encoding Toll-like receptor 4 (TLR4), the transcription factor NFkB1, the chemokine
interleukin 8 (IL8), inflammatory cytokines (interleukins IL1β, IL6; tumour necrosis factor,
TNF), β-defensins (lingual antimicrobial peptides LAP, tracheal antimicrobial peptide TAP) and
acute phase proteins (haptoglobin, HP; serum amyloid A, SAA3) was examined in endometrial
epithelial cells stimulated with E. coli for 6 and 24 h using qRT-PCR. Expression of all genes
was increased significantly (P < 0.05) 6 h post-stimulation. Expression of IL1b, TNF and SAA3
genes was increased by 121-, 357- and 721-fold, respectively (P < 0.05). Twenty four hours
post-stimulation, IL1b, IL6, IL8, TNF and LAP gene expression was decreased compared to 6 h,
whereas TAP and SAA3 expression was further increased to 209- and 3452-fold (P < 0.05). E.
coli driven expression of immune effector genes demonstrates potent immune, antimicrobial and
regulatory capacity of endometrial epithelial cells to respond to this pathogen.