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Published on: January 6, 2012
Prostaglandin E2 accumulation is closely associated with S. aureus-infected bovine endometritis
1School of Public Healthy, Inner Mongolia Medical University, 010110 Hohhot, China; Laboratory of Veterinary Pharmacology, College of Veterinary Medicine, Inner Mongolia Agricultural University, 010018 Hohhot, China.
Abstract:
S. aureus isolated from bacterial bovine endometritis is common in epidemiological reports, but is often ignored as a subclinical pathogenic microorganism. In a previous study, we showed that live S. aureus (LSA) and heat killed S. aureus (HK-SA) induce different inflammatory responses in bovine endometrial tissue, and possibly being associated with the accumulation of prostaglandin E2 (PGE2). Thus, in this study, we varied PGE2 concentrations using inhibitors or agonists in HK-SA-treated bovine endometrial tissues. The results demonstrated that PGE2 has a positive relationship with IL-6, TNF-α, and damage-associated molecular patterns (DAMPs; e.g., HMGB-1 and HABP-1) expression and tissues damage, and is regulated by the EP4-p38 MAPK pathway. We concluded that lipoproteins of S. aureus are associated with PGE2 generation. To further explore the relationship between LSA and PGE2 accumulation, we used the S. aureus strain SA113 lipoprotein knockout (SA113Δlpl) to infect bovine endometrial epithelial cells (BECs). LSA decreased PGE2, cAMP, EP4, IL-6, IL-8, cAMP secretion, and the MAPK and PKA signaling pathways when infected with SA113Δlpl, as compared with SA113-infected groups. Moreover, the adhesion and invasion of BECs were similarly downregulated when lipoproteins in S. aureus were knocked out. The results of this study show that PGE2 is involved in both HK-SA- and LSA-induced inflammatory responses in the bovine endometrium. We suggest that S. aureus infection is associated with bovine endometritis, and although HK-SA and LSA induce different inflammatory responses, the strategy of decreasing PGE2 accumulation is helpful in reducing the inflammation stage caused by S. aureus.
Insights
Prostaglandin E2 (PGE2) plays a key role in bovine endometritis caused by Staphylococcus aureus. Reducing PGE2 accumulation effectively mitigates inflammation from both live and killed S. aureus infections.
Area of Science:
- Veterinary Immunology
- Bacterial Pathogenesis
- Reproductive Immunology
Background:
- Staphylococcus aureus is a common cause of bovine endometritis, often overlooked as a subclinical pathogen.
- Previous work indicated live S. aureus (LSA) and heat-killed S. aureus (HK-SA) elicit distinct inflammatory responses in bovine endometrium, potentially linked to prostaglandin E2 (PGE2) accumulation.
Purpose of the Study:
- To investigate the role of PGE2 in HK-SA-induced inflammation in bovine endometrial tissues.
- To explore the relationship between LSA, PGE2, and inflammatory pathways in bovine endometrial epithelial cells (BECs).
- To determine the impact of S. aureus lipoproteins on PGE2 generation and cellular responses.
Main Methods:
- Varying PGE2 concentrations using inhibitors/agonists in HK-SA-treated bovine endometrial tissues.
- Infecting BECs with S. aureus strain SA113 and its lipoprotein knockout mutant (SA113Δlpl).
- Measuring inflammatory markers (IL-6, TNF-α, DAMPs), signaling pathways (MAPK, PKA), and cellular functions (adhesion, invasion).
Main Results:
- PGE2 positively correlated with IL-6, TNF-α, DAMPs (HMGB-1, HABP-1), and tissue damage, regulated by the EP4-p38 MAPK pathway.
- S. aureus lipoproteins are associated with PGE2 generation.
- LSA infection with SA113Δlpl decreased PGE2, cAMP, EP4, IL-6, IL-8, and MAPK/PKA signaling compared to SA113 infection.
- Lipoprotein knockout also downregulated BEC adhesion and invasion.
Conclusions:
- PGE2 is integral to both HK-SA- and LSA-induced inflammatory responses in the bovine endometrium.
- S. aureus infection contributes to bovine endometritis.
- Targeting PGE2 accumulation is a potential therapeutic strategy to reduce S. aureus-induced inflammation, irrespective of bacterial viability.
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