Bronchopulmonary dysplasia of the premature baby : An immunohistochemical study

• Published in: Pediatric pulmonology Vol. 24; no. 1; pp. 22 - 28
• Main Authors: TOTI, P, BUONOCORE, G, TANGANELLI, P, CATELLA, A. M, PALMERI, M. L. D, VATTI, R, SEEMAYER, T. A
• Format: Journal Article
• Language: English
• Published: New York, NY Wiley-Liss 01-07-1997
• Subjects: Acute Disease; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Bronchopulmonary Dysplasia - metabolism; Bronchopulmonary Dysplasia - pathology; Chronic Disease; Emergency and intensive care: neonates and children. Prematurity. Sudden death; Fibroblasts - pathology; Fibroblasts - physiology; Gestational Age; Humans; Immunohistochemistry; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases - metabolism; Infant, Premature, Diseases - pathology; Intensive care medicine; Lung - metabolism; Lung - pathology; Medical sciences; Pulmonary Alveoli - pathology; Transforming Growth Factor beta - physiology; Immunohistochemistry; Premature; Lung disease; Dysplasia; Respiratory disease; Transforming growth factor β; Myofibroblast; Respiratory intensive care; Exploration; Hyaline membrane; Artificial ventilation; Bronchopulmonary; Pathology; Autopsy; Bronchus disease; Respiratory distress; Complication
• ISSN: 8755-6863; 1099-0496
• DOI: 10.1002/(SICI)1099-0496(199707)24:1<22::AID-PPUL4>3.0.CO;2-L

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.