Abstract
Streptococcus uberis is frequently isolated from the mammary gland of dairy cattle. Infection with some strains can induce mild subclinical inflammation whilst others induce severe inflammation and clinical mastitis. We compared here the inflammatory response of primary cultures of bovine mammary epithelial cells (pbMEC) towards S. uberis strains collected from clinical or subclinical cases (seven strains each) of mastitis with the strong response elicited by Escherichia coli. Neither heat inactivated nor live S. uberis induced the expression of 10 key immune genes (including TNF, IL1B, IL6). The widely used virulent strain 0140J and the avirulent strain, EF20 elicited similar responses; as did mutants defective in capsule (hasA) or biofilm formation (sub0538 and sub0539). Streptococcus uberis failed to activate NF-κB in pbMEC or TLR2 in HEK293 cells, indicating that S. uberis particles did not induce any TLR-signaling in MEC. However, preparations of lipoteichoic acid (LTA) from two strains strongly induced immune gene expression and activated NF-κB in pbMEC, without the involvement of TLR2. The immune-stimulatory LTA must be arranged in the intact S. uberis such that it is unrecognizable by the relevant pathogen receptors of the MEC. The absence of immune recognition is specific for MEC, since the same S. uberis preparations strongly induced immune gene expression and NF-κB activity in the murine macrophage model cell RAW264.7. Hence, the sluggish immune response of MEC and not of professional immune cells to this pathogen may aid establishment of the often encountered belated and subclinical phenotype of S. uberis mastitis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-015-0287-8) contains supplementary material, which is available to authorized users.
Highlights
The Gram-positive bacterium Streptococcus uberis is among the four most prevalent species of mastitis causing pathogens [1, 2]
Streptococcus uberis failed to elicit TLR2 signaling and NF‐κB activation in Mammary epithelial cells (MEC) We examined if a lack of toll-like receptor (TLR) activation might be the underlying cause for the absence of any immune gene activation in MEC
We investigated if other components of the S. uberis strain 233 cell envelope might activate nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) factors in primary cultures of bovine mammary epithelial cells (pbMEC)
Summary
The Gram-positive bacterium Streptococcus uberis is among the four most prevalent species of mastitis causing pathogens [1, 2] Infection with this bacterium can occur with very few if any clinical signs, but can result in severe inflammation of the udder culminating in clinical mastitis [3]. No clear gene-loss or -gain correlation with the virulent or avirulent phenotype of the strains emerged in a very recent comparison of the whole genome sequences from thirteen different S. uberis strains [5]. This suggests that the particular outcome of an udder infection
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