| Type I and III procollagen propeptides in sarcoidosis, fibrosing alveolitis and asbestos-related lung diseases | ||
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Normal alveolar walls and the surrounding capillaries showed procollagen I aminoterminal propeptide positivity in linear and continuous fibres. Detectable immunoreactivity for PINP was found in the middle of the interstitium of the alveolar walls (see Image 1, panel A in paper IV). The bronchiolar walls contained immunoreactivity for PINP within the connective tissue that separates the smooth muscle into bundles (see Image 1, panel C in paper IV). PINP could be detected in the tunica media layer of both arteries and veins. In visceral pleura, faint PINP immunopositivity was seen in the area between the submesothelial layer of the pleura and the alveoli of the lung.
The staining for procollagen III aminoterminal propeptide within the alveolar walls appeared to be stronger and the distribution was different from that seen in the immunoreactivity for PINP (see Image 1 in paper IV). PIIINP was localised near the epithelial cells lining alveolar walls and the cells in the interstitium, giving a spiral appearance (see Image 1, panel B in paper IV). PIIINP was also detected around the capillaries very close to the BM. PIIINP was further expressed in the bronchioli as intensive linear fibres underneath the basement membrane (see Image 1, panel D in paper IV). Furthermore, immunoreactivity of PIIINP was seen in the tunica intima, media and adventitia layers of both arteries and veins. PIIINP was also expressed as linear fibres in the pleura underneath the BM of detached mesothelial cells. Fainter immunoreactivity was detected in the same area as PINP, i. e. between the submesothelial layer of the pleura and the alveoli of the lung. No intracellular immunoreactivity for PINP or PIIINP was seen in normal lung.
Immunoreactivity for PINP was detected mainly within granulomas in sarcoidosis. It was exhibited as intracellular granular spots localising mainly in the area between the epitheloid cells and the lymphocytes (see Image 4 in paper IV). Occasionally, giant cells in granulomas expressed immunoreactivity for PINP.
PIIINP was exhibited mainly as extracellular linear and reticular fibres around the granulomas, not as intracellular spots similar to PINP (see Image 4 in paper IV). Some faint fibres were also seen in the inner parts of granulomas. The extracellular immunoreactivity for PIIINP was stronger than that for PINP around the lymphocytes outside granulomas. Intracellular immunoreactivity for PIIINP was not found in sarcoidosis.
Immunoreactivity for PINP was observed in areas of recent epithelial damage both intracellularly and in the extracellular space in usual interstitial pneumonia. Intracellular PINP was expressed mainly in the newly formed fibrosis, i.e. fibroblast foci, as intracellular spots within fibroblasts and myofibroblasts (see Image 2 in paper IV). The extracellular expression for PINP was strongest in the areas of ongoing epithelial regeneration with type II pneumocytes (see Images 2 and 3 in paper IV). Faint immunoreactivity of PINP could be detected extracellularly underneath the totally regenerated epithelium with type II pneumocytes or metaplastic bronchiolar-type cells (see Image 3 in paper IV). Occasionally, some immunoreactivity for PINP was also detected as short extracellular fibres. Furthermore, newly developed fibrosis within alveolar walls in areas of ongoing remodelling and in intra-alveolar and incorporating fibrosis contained remarkable positivity for PINP immunoreactivity intracellularly (see Image 2, panel C in paper IV). In some cases, linear and reticular immunopositivity for PINP was observed around alveolar macrophages (see Image 3, panel E in paper IV).
Procollagen III aminoterminal propeptide was expressed mainly as extracellular linear fibres underneath the BM of the regenerated epithelium. The immunoreactivity for PIIINP was observed in both intra-alveolar and incorporating fibrosis (see Image 2 in paper IV). Immunoreactivity for PIIINP was most intense in the areas of regenerated metaplastic alveolar epithelium or bronchiolar-type epithelium (see Image 3 in paper IV), while, unlike PINP, it was not expressed in recent epithelial damage. In these areas, faint and slim immunopositive fibres for PIIINP were located underneath the BM. The immunoreactivity for PIIINP, though not for PINP, was exhibited marginally around lymphocytes. The expression of PIIINP was detected around clusters of intra-alveolar macrophages, as was the case with PINP (see Image 3, panels E and F in paper IV). Immunoreactivity for PIIINP was not seen intracellularly in fibrosing alveolitis.