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Ureaplasma parvum infection induces inflammatory changes in vaginal epithelial cells independent of sialidase
Emmanuel Amabebe1, Lauren S Richardson2, Giovana Fernanda Cosi Bento2,3
1Department of Oncology and Metabolism, University of Sheffield, Sheffield, UK.
Background:
Ureaplasma, a genus of the order Mycoplasmatales and commonly grouped with Mycoplasma as genital mycoplasma is one of the most common microbes isolated from women with infection/inflammation-associated preterm labor (PTL). Mycoplasma spp. produce sialidase that cleaves sialic acid from glycans of vaginal mucous membranes and facilitates adherence and invasion of the epithelium by pathobionts, and dysregulated immune response. However, whether Ureaplasma species can induce the production of sialidase is yet to be demonstrated. We examined U. parvum-infected vaginal epithelial cells (VECs) for the production of sialidase and pro-inflammatory cytokines.
Methods:
Immortalized VECs were cultured in appropriate media and treated with U. parvum in a concentration of 1 × 105 DNA copies/ml. After 24 h of treatment, cells and media were harvested. To confirm infection and cell uptake, immunocytochemistry for multi-banded antigen (MBA) was performed. Pro-inflammatory cytokine production and protein analysis for sialidase confirmed pro-labor pathways.
Results:
Infection of VECs was confirmed by the presence of intracellular MBA. Western blot analysis showed no significant increase in sialidase expression from U. parvum-treated VECs compared to uninfected cells. However, U. parvum infection induced 2-3-fold increased production of GM-CSF (p = 0.03), IL-6 (p = 0.01), and IL-8 (p = 0.01) in VECs compared to controls.
Conclusion:
U. parvum infection of VECs induced inflammatory imbalance associated with vaginal dysbiosis but did not alter sialidase expression at the cellular level. These data suggest that U. parvum's pathogenic effect could be propagated by locally produced pro-inflammatory cytokines and, unlike other genital mycoplasmas, may be independent of sialidase.
Insights
Ureaplasma parvum infection in vaginal cells increases inflammatory cytokines but not sialidase. This suggests U. parvum may cause preterm labor through inflammation, independent of sialidase activity.
Area of Science:
- Reproductive biology
- Microbiology
- Immunology
Background:
- Ureaplasma is a common genital mycoplasma linked to preterm labor (PTL).
- Mycoplasma species can produce sialidase, aiding pathogen invasion and immune dysregulation.
- The role of Ureaplasma parvum in inducing sialidase production remains unclear.
Purpose of the Study:
- To investigate if Ureaplasma parvum infection stimulates sialidase production in vaginal epithelial cells (VECs).
- To assess the impact of U. parvum infection on pro-inflammatory cytokine production in VECs.
Main Methods:
- Vaginal epithelial cells (VECs) were infected with Ureaplasma parvum (1×10⁵ DNA copies/ml).
- Immunocytochemistry confirmed U. parvum infection and cell uptake via multi-banded antigen (MBA).
- Western blot analyzed sialidase expression; cytokine levels (GM-CSF, IL-6, IL-8) were measured.
Main Results:
- Ureaplasma parvum infection was confirmed within VECs.
- No significant increase in sialidase expression was observed in infected VECs.
- U. parvum infection led to a 2-3 fold increase in GM-CSF, IL-6, and IL-8 production.
Conclusions:
- Ureaplasma parvum infection induces an inflammatory imbalance in VECs, contributing to vaginal dysbiosis.
- Sialidase expression is not significantly altered by U. parvum at the cellular level.
- U. parvum's pathogenic role in PTL may be mediated by pro-inflammatory cytokines, independent of sialidase.
