Research Paper Volume 8, Issue 11 pp 3091—3109

The role of club cell phenoconversion and migration in idiopathic pulmonary fibrosis

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Figure 5. Aberrant α-SMA signals are frequently encountered in the vicinity of disorganized Claudin-10-positive cells in IPF lungs. IPF and DIP lung sections were immunohistochemically double-labeled for Cldn10 and α-SMA. Brown and blue signals correspond to Cldn10 and α-SMA respectively. (B, E, H, K, N) are magnified views of the boxed regions in (A, D, G, J, M) respectively. (C, F, I, L, O) are magnified views of the boxed regions in (B, E, H, K, N) respectively. (A, B, C) Representative photomicrographs from DIP lungs are shown. α-SMA signals are largely spotted beneath the arterial walls, where smooth muscle cells typically reside. No aberrant proximity is seen between Cldn10-positive cells and α-SMA signals. (D, E, F) Fibrotic interstitium showing aberrant α-SMA signals in close proximity to Cldn10-positive club cells. Note the juxtaposition of Cldn10-negative cuboidal cells with Cldn10-positive cells and aberrant α-SMA signals (F). (G, H, I) Mosaic cell masses containing Cldn10-positive and negative cells are floating in an enlarged airspace. Cldn10-positive club cells infiltrating the fibrotic interstitium (I). (J, K, L) Cldn10-positive club cells form multilayers in bronchiolar epithelium (L) in close proximity to intense α-SMA signals (K). (M, N, O) Boundary region between normal-looking alveoli and moderately affected area with thickened interstitium is shown. Areas surrounded by dashed lines denote mosaic cell masses containing Cldn10-positive and negative cells. Apparently, those cell masses have occluded the alveolar airspaces. Original magnifications: x40 (A, D, G, J); x100 (B, E, H, K, M); x200 (N); x100 (C, F, I, L, O).