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Published ahead of print on June 13, 2003, doi:10.1164/rccm.200212-1434OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 601-611, (2003)
© 2003 American Thoracic Society

Original Article

Bombesin-like Peptides and Mast Cell Responses

Relevance to Bronchopulmonary Dysplasia?

Meera Subramaniam, Kumiya Sugiyama, David H. Coy, Yanping Kong, York E. Miller, Peter F. Weller, Keiji Wada, Etsuko Wada and Mary E. Sunday

Department of Pathology and Pulmonology, Children's Hospital Boston; Department of Medicine, Harvard Thorndike Laboratories, Charles A. Dana Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical School; and Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts; Department of Medicine, Peptide Research, Tulane University Health Sciences, New Orleans, Louisiana; Department of Medicine, Veterans Affairs Medical Center, University of Colorado, Denver, Colorado; and Institute of Neuroscience, Tokyo, Japan

Correspondence and requests for reprints should be addressed to Mary E. Sunday, M.D., Ph.D., Brigham and Women's Hospital, Department of Pathology, 75 Francis Street, Boston, MA 02115. E-mail: sunday{at}tch.harvard.edu

Bombesin-like peptides (BLPs) are elevated in newborns who later develop bronchopulmonary dysplasia (BPD). In baboon models, anti-BLP blocking antibodies abrogate BPD. We now demonstrate hyperplasia of both neuroendocrine cells and mast cells in lungs of baboons with BPD, compared with non-BPD controls or BLP antibody-treated BPD baboons. To determine whether BLPs are proinflammatory, bombesin was administered intratracheally to mice. Forty-eight hours later, we observed increased numbers of lung mast cells. We analyzed murine mast cells for BLP receptor gene expression, and identified mRNAs encoding bombesin receptor subtype 3 and neuromedin-B receptor (NMB-R), but not gastrin-releasing peptide receptor. Only NMB-R-null mice accumulated fewer lung mast cells after bombesin treatment. Bombesin, gastrin-releasing peptide, NMB, and a bombesin receptor subtype 3-specific ligand induced mast cell proliferation and chemotaxis in vitro. These observations support a role for multiple BLPs in promoting mast cell responses, suggesting a mechanistic link between BLPs and chronic inflammatory lung diseases.

Key Words: bronchopulmonary dysplasia • chemotaxis • infant, premature • neuromedin B • pulmonary fibrosis




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