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Bronchopulmonary dysplasia of the premature baby: an immunohistochemical study
P Toti1, G Buonocore, P Tanganelli
1Institute of Pathology, University of Siena, Italy.
Insights
Myofibroblasts are key cells in premature lung repair, increasing after injury and potentially converting to smooth muscle. Transforming growth factor-beta (TGF-beta) influences their activity, suggesting therapeutic targets for bronchopulmonary dysplasia (BPD).
Area of Science:
- Neonatal Medicine
- Pulmonary Biology
- Cellular Biology
Background:
- Premature infants on ventilation risk chronic lung disease, including bronchopulmonary dysplasia (BPD).
- The specific cells mediating repair in the premature lung remain poorly understood.
- Fibroblast activation into myofibroblasts is crucial for tissue repair, regulated by cytokines like TGF-beta.
Purpose of the Study:
- To identify and characterize the cells involved in the repair process of premature lungs.
- To investigate the role of myofibroblasts and TGF-beta in lung injury repair in neonates.
Main Methods:
- Immunocytochemical analysis of lung tissue from 39 premature infants with neonatal respiratory distress syndrome (RDS).
- Utilized antibodies against vimentin, alpha-smooth muscle (alpha-SM) actin, desmin, MAC387, and TGF-beta.
- Examined cellular changes following mechanical ventilation and oxygen therapy.
Main Results:
- Myofibroblasts are normally present in developing lungs and increase post-injury.
- These cells form bundles around air spaces and acquire desmin, suggesting smooth muscle metaplasia.
- Myofibroblast proliferation and migration correlate with TGF-beta presence.
Conclusions:
- Myofibroblasts play a significant role in premature lung repair mechanisms.
- TGF-beta appears to regulate myofibroblast activity in injured neonatal lungs.
- Targeting TGF-beta or related cytokines may offer therapeutic strategies to prevent BPD.
Abstract:
Prematurely born infants who required assisted ventilation may develop chronic lung disease or bronchopulmonary dysplasia (BPD). The cells involved in the reparative process of the premature lung are not well defined. The repair of injured tissues is a highly standardized process and the most important cells are activated (modulated) fibroblasts (myofibroblasts). A key cytokine in controlling repair is transforming growth factor-beta (TGF-beta). To characterize the cells involved in the repair process of the premature lung, we employed immunocytochemical techniques and examined the lungs of 39 autopsied premature babies who had neonatal respiratory distress syndrome (RDS). All were treated in neonatal intensive care units and required mechanical ventilation and supplemental oxygen; all survived for at least 12 hours. Antibodies were employed against vimentin, alpha-smooth muscle (alpha-SM) actin, total muscle actin, desmin, MAC387, and TGF-beta. Our study indicates that myofibroblasts are normally present along terminal airways in the developing lung. These cells increase in number some days after lung injury, form bundles of cells encircling terminal air spaces, and acquire desmin contractile filaments shortly thereafter. Myofibroblasts do not lose their contractile filaments with time, suggesting a conversion to smooth muscle metaplasia. The proliferation and migration of such myofibroblasts at sites of lung injury is associated with the presence of TGF-beta. These findings suggest that myofibroblasts play an important role in premature lung repair. They may point the way to experimental and clinical trials that will identify drugs antagonistic to TGF-beta (or other cytokines). Such antagonists may protect the neonates who are at high risk of developing BPD.