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Growth of putative progenitors of type II pneumocytes in culture of human cystic fibrosis alveoli
Author(s) -
Hollande Etienne,
Cantet Sylvie,
Ratovo Ginette,
Daste Ghislaine,
Brémont Franc¸ois,
Fanjul Marjorie
Publication year - 2004
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/j.biolcel.2004.04.005
Subject(s) - biology , cytokeratin , lamellar granule , pathology , progenitor cell , cuboidal cell , alveolar epithelium , population , epithelium , microbiology and biotechnology , immunology , stem cell , anatomy , immunohistochemistry , medicine , genetics , environmental health , ultrastructure
Summry— Alveolar type II pneumocytes are thought to be progenitor cells capable of self‐renewal and differentiation into type I pneumocytes. Nevertheless, the existence of an alveolar stem cell has been postulated. In lungs from patients with cystic fibrosis, the alveolar epithelium is damaged with ulceration and subsequent regeneration. We characterized alveolar modifications histologically and immunohistochemically in the pulmonary tissue of a patient homozygous for the ΔF508 mutation. Alveoli were of variable size and surrounded by an inflammatory infiltrate. They were lined by a continuous layer of cuboidal cells with very weak proliferative activity. These cells resembled type II pneumocytes. They expressed thyroid transcription factor‐1, cystic fibrosis transmembrane conductance regulator, cytokeratin 7 and contained lamellar bodies. Weak expression of cytokeratin 5 considered to be a marker of progenitor cells of the bronchial and bronchiolar epithelium was detected. Explantation of this alveolar epithelium produced primary cultures and subcultures of epithelial cells that had acquired proliferative properties showing signs of dedifferentiation with a loss of lamellar bodies and a lack of expression of thyroid transcription factor‐1. Persistence of the expression of cytokeratin 7 and a strong expression of cytokeratin 5 were observed. The culture conditions were thought to have circumvented the inhibition of proliferation observed in vivo due to the inflammatory peri‐alveolar environment. They thus favored the multiplication of a population of cells co‐expressing cytokeratin 5 and certain characteristics of type II pneumocytes. The presence of these cells of intermediate phenotype is indicative of the existence of immature precursors for type II pneumocytes.

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