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A study was carried out to obtain a more detailed picture of the phenotypes of human otosclerotic and normal bone cells and to analyse the response of both populations to treatment with TGF beta 1. Total collagen synthesis was found to be decreased, but fibronectin secretion increased in otosclerotic with respect to normal cells. Although overall glycosaminoglycan (GAG) synthesis was lower in otosclerotic cells, the sulphated GAG to hyaluronic acid (HA) ratio was higher, in particular there was greater expression of chondroitin (CS) and dermatan sulphates (DS). TGF beta 1 induced a more marked increase in collagen and fibronectin release and greater production of sulphated GAGs as DS and heparan sulphate (HS) in the otosclerotic cells. The fact that the phenotype of the otosclerotic cells differed from that of the normal cells and could be modified by TGF beta 1 treatment, suggests that TGF beta 1 is implicated in the pathogenesis of otosclerosis.

This paper investigates the ability of macrophages and of non-typically phagocitic cells such as fibroblasts to internalize 51Cr-labelled C. albicans in presence or in absence of lectin concanavalin A (Con A). The results obtained demonstrate that fibroblasts are also able to internalize C. albicans and that this property is potentiated by the presence of Con A. Lectin modifies only the phenotype of the fibroblast, which, poorly attached to the substrate, is globular in shape. Despite reduced cellular spreading, phagocytosis is stimulated by the lectin. In both cell populations, changes in the organization of some cytoskeletal proteins such as tubulin, actin and alpha-actinin are evident during the C. albicans infection; such rearrangements are more evident and longlasting in the fibroblasts treated with Con A.

Conditioned medium (CM), collected from 7 and 14 days-old chick embryo skin fibroblasts and added to the same cells, increases glycosaminoglycans (GAG) intra- and extracellular accumulation. The factors responsible for GAG enhancement are TGF alpha and TGF beta because they are trypsin and dithiothreitol sensitive, stable or enhanced by heat and transient acidification. Moreover, Sephadex G-75 fractions of CM active on GAG synthesis contain, when analysed on SDS-polyacrylamide gel electrophoresis, two bands that comigrate with TGF alpha and TGF beta and induce NRK cells clone 49F to form large colonies of mean size > 8.000 microns 2 in soft agar. Since both the factors must be present to induce the formation of large colonies we come to the conclusion that CM contains TGF alpha and TGF beta. The two growth factors have different effects on the accumulation of individual classes of GAG in the ECM. In particular, TGF beta stimulates a marked increase of CS and DS, TGF alpha of HA and DS in the medium. The contemporaneous addition of TGF alpha and TGF beta to 7 days-old fibroblasts produces a pattern of GAG response similar to CM. These embryonic fibroblasts may control their own GAG synthesis and secretion through autocrine TGF alpha and beta activity.