Background Development 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 Methods Tracheal 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. Results U. 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. Conclusion Both 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 <UnorderedList Mark="Bullet"> <ItemContent> U. urealyticum and U. parvum can contribute to the inflammation and cell damage seen in chronic lung disease through the secretion of inflammatory mediators. </ItemContent> <ItemContent> 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. </ItemContent> <ItemContent> Our data provide new insights into the role of Ureaplasma in the development of chronic lung disease in premature infants. </ItemContent> </UnorderedList>

Ureaplasma parvum and Ureaplasma urealyticum induce distinct types of inflammation in neonates and human epithelial cell models

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2025年10月3日

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Hongzhen Zhu,
Pol Oliveras-Julià,
Gea F. Hasperhoven,
Luca L. van Leeuwen,
Ad C. J. M. de Bruijn,
Marijn C. Verwijs,
Annemarie M. C. van Rossum,
René F. Kornelisse,
Kim Stol,
Wendy W. J. Unger

摘要

Background

Development 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

Methods

Tracheal 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.

Results

U. 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.

Conclusion

Both 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.