ArticlePediatric research2026
Ureaplasma parvum and Ureaplasma urealyticum induce distinct types of inflammation in neonates and human epithelial cell models.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The role of Ureaplasma in preterm lung disease: does species matter?Pediatric research · 2026Article
- Early antibiotic exposure and the risk of necrotizing enterocolitis in preterm neonates: insights from a large multicenter cohort in China.Pediatric research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDevelopment of bronchopulmonary dysplasia (BPD) in premature neonates is associated with infection and inflammation. Both Ureaplasma parvum and Ureaplasma urealyticum are associated with BPD. We examined whether there is a difference in pathogenicity between the two species
methodsTracheal aspirates of 25 preterm neonates were analyzed for bacterial presence and inflammatory mediators. Alveolar epithelial cells were infected with U. parvum and U. urealyticum strains to assess inflammatory mediators, cell death and oxidative stress.
resultsU. parvum was detected in 2/25 and U. urealyticum in another 3/25 neonates. E. coli was co-detected in 3/5 Ureaplasma-positive samples. U. parvum-positive samples contained high IL-6, IL-8 and CXCL5. U. urealyticum-positive samples also contained high IL-6 and IL-8, but low CXCL5, and high CXCL1 and CCL2. Five-to-ten-fold higher IL-6 and two-fold higher IL-8 levels were detected in U. parvum-infected cell cultures than U. urealyticum, whereas apoptotic cell death was detected in U. urealyticum-infected cultures. Infection with both species induced ROS.
conclusionBoth Ureaplasma species may contribute to inflammation and cell damage, via oxidative stress, as observed in BPD, yet through different mechanisms. U. parvum infection induces a strong pro-inflammatory mediator response in alveolar epithelial cells while U. urealyticum infection results in cell death. IMPACT: U. urealyticum and U. parvum can contribute to the inflammation and cell damage seen in chronic lung disease through the secretion of inflammatory mediators. The two species differ in their mechanism of action: U. parvum infection induces a strong pro-inflammatory mediator response in alveolar epithelial cells while U. urealyticum infection results in epithelial cell death. Our data provide new insights into the role of Ureaplasma in the development of chronic lung disease in premature infants.
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