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Updated: Aug 7, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Disordered pulmonary myofibroblast distribution and elastin expression in preterm infants with Ureaplasma urealyticum
Rose Viscardi1, Winston Manimtim, Ju Ren He
1Department of Pediatrics, University of Maryland School of Medicine, 22 South Greene Street, Baltimore, 21201, USA. rviscard@umaryland.edu
Insights
Ureaplasma infection in preterm infants causes lung fibrosis and abnormal elastin development, contributing to bronchopulmonary dysplasia. This study details the molecular mechanisms behind this severe lung disease.
Area of Science:
- Neonatal pathology
- Pulmonary medicine
- Microbiology
Background:
- Ureaplasma urealyticum colonization is a key risk factor for bronchopulmonary dysplasia (BPD) in preterm infants.
- BPD involves impaired alveolar development, interstitial fibrosis, and disordered elastic fibers in the distal lung.
- Previous studies highlight fibrosis as a characteristic of Ureaplasma-induced lung injury in preterm neonates.
Purpose of the Study:
- To investigate the preterm lung's specific response to Ureaplasma infection.
- To characterize the cellular and molecular changes associated with Ureaplasma-related lung pathology.
- To elucidate the role of alpha-smooth muscle actin (alphaSMA), transforming growth factor beta1 (TGFbeta1), and elastin expression in Ureaplasma-induced lung injury.
Main Methods:
- Analysis of lung specimens from preterm infants: 4 gestational controls (GC), 12 with other pneumonia, and 5 with Ureaplasma infection.
- Immunohistochemistry for alphaSMA and TGFbeta1.
- Hart's elastin staining and in situ hybridization for tropoelastin (TE) expression.
Main Results:
- Ureaplasma and other pneumonia cases showed increased alphaSMA-positive myofibroblasts around terminal airspaces compared to controls, correlating with fibrosis severity.
- TGFbeta1 immunostaining was elevated in alveolar macrophages in Ureaplasma-infected lungs compared to other pneumonia cases.
- Ureaplasma infection led to extensive elastic fiber accumulation and widespread TE expression in terminal airspaces, linked to ventilation duration.
Conclusions:
- Ureaplasma infection is associated with increased TGFbeta1 in alveolar macrophages and myofibroblast proliferation, driving abnormal lung septation and fibrosis.
- The study reveals a prolonged and pronounced elastogenic response in the preterm lung following Ureaplasma exposure.
- These findings underscore Ureaplasma's significant contribution to the pathogenesis of bronchopulmonary dysplasia through specific molecular and cellular alterations.
Abstract:
Respiratory colonization of preterm infants with Ureaplasma urealyticum is a significant risk factor for bronchopulmonary dysplasia, a chronic lung disease characterized by arrest of alveolar development, variable interstitial fibrosis, and disordered elastic fibers in the distal airspaces. As indicated in previous studies, moderate to severe fibrosis is a hallmark of pathology in the Ureaplasma-infected preterm lung. To further characterize the preterm lung's response to Ureaplasma, lung specimens from 4 gestational controls (GC), 12 other pneumonia and 5 Ureaplasma-infected infants were analyzed by immunohistochemistry for alpha-smooth muscle actin (alphaSMA) and transforming growth factor beta1 (TGFbeta1), Hart's elastin staining, and in situ hybridization for tropoelastin (TE) expression. Cells positive for alphaSMA were observed in thickened, extensive bundles surrounding terminal airspaces in Ureaplasma and other pneumonia cases compared to individual myofibroblasts in GC. The myofibroblast pattern correlated with the severity of fibrosis, but not duration of ventilation. Transforming growth factor beta1 immunostaining was primarily localized to alveolar macrophages and was increased in Ureaplasma more than in other pneumonia cases. Elastic fibers and TE-expressing cells were spatially limited to emerging septal tips in GC. In pneumonia cases, increased deposition of elastic fibers was observed surrounding terminal airspaces, but TE expression was similar to GC. In Ureaplasma specimens, accumulation of elastic fibers correlated with duration of ventilation, and TE expression was extensive throughout the walls of terminal airspaces. These findings suggest that Ureaplasma is associated with alveolar macrophage TGFbeta1 immunostaining and myofibroblast proliferation contributing to abnormal septation, interstitial fibrosis, and a prolonged and strong elastogenic response in the preterm lung.
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