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Ureaplasma urealyticum induces apoptosis in human lung epithelial cells and macrophages
Ying-Hua Li1, Ming Chen, Annelie Brauner
1Neonatal Unit, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden. ying-hua.li@kbh.ki.se
Insights
Ureaplasma urealyticum may contribute to chronic lung disease (CLD) in premature infants by inducing cell death in lung epithelial cells and macrophages. This infection could impair lung structure and the host immune response, worsening CLD development.
Area of Science:
- Neonatal respiratory health
- Infectious disease mechanisms
- Cellular apoptosis
Background:
- Chronic lung disease (CLD) of prematurity is a major cause of infant morbidity.
- CLD involves inflammation, cell damage, and debated roles of infections like Ureaplasma urealyticum.
- Apoptosis of lung cells has been observed in CLD and bronchopulmonary dysplasia.
Purpose of the Study:
- To investigate the role of Ureaplasma urealyticum in inducing apoptosis in lung cells.
- To determine if Ureaplasma urealyticum contributes to the pathogenesis of CLD in premature infants.
Main Methods:
- Induction of apoptosis in human lung epithelial cells (A549) and macrophages (THP-1) using Ureaplasma urealyticum.
- Assessment of apoptosis via phosphatidylserine translocation, DNA fragmentation, cell morphology, and cell viability assays.
- Evaluation of anti-TNF-alpha antibody's protective effect on macrophages.
Main Results:
- Ureaplasma urealyticum infection induced apoptosis in both lung epithelial cells and macrophages.
- Apoptosis was confirmed through multiple assays including flow cytometry, DNA fragmentation, and morphological changes.
- Anti-TNF-alpha antibody offered partial protection to macrophages against Ureaplasma-induced apoptosis.
Conclusions:
- Ureaplasma urealyticum may play a role in the development of CLD by triggering apoptosis in key lung cells.
- The findings suggest Ureaplasma urealyticum could impair lung structure and the host immune response in premature infants.
- Targeting inflammatory pathways like TNF-alpha might be a potential therapeutic strategy.
Abstract:
Chronic lung disease (CLD) of prematurity remains a significant cause of morbidity among premature infants. It is a multifactorial disorder and characterized by an early increased number of neutrophils and alveolar macrophages, with later architectural epithelial and endothelial cell damage. Recently, apoptosis of type 2 pneumocytes in the lung of preterm neonates with acute and chronic lung disease has been examined and apoptosis of mesenchymal cells was detected in the chronic stage of bronchopulmonary dysplasia. Infection and inflammatory responses in the lungs play important roles. However, the contribution of Ureaplasma urealyticum to the development of CLD is debated. We found that U. urealyticum induced apoptosis in human type II lung epithelial cells (A549 cell line) and macrophages (derived from human monocytic cell line THP-1) by measuring the outer leaflets translocation of phosphatidylserine (flow cytometry analysis and fluorescence microscopy assessment), DNA fragmentation analysis, cell morphology changes such as diminution in cell volume, increased cytoplasmic staining, and nuclear pyknosis (hematoxylin and eosin staining) and viable counting (trypan blue exclusion). Anti-TNF-alpha monoclonal antibody partially protected the macrophages from undergoing apoptosis after infection with U. urealyticum. Our findings imply that U. urealyticum might be involved in impairing lung structure and host immune response during the development of CLD.