Assessment of mechanical- stress induced by deposited hbrors particles on the wall in rhythmically expanding al.vf-oll

Current investigations of cytotoxicit\ caused by deposited fibrous particles te r asbestos) -ire centered un cytocliemical response. However, main inhaled particles are actually chemically inert, \'et harmful We hypothesize that the contact of fibrous particle with the alveolar epithelium causes mechanical damage on the ceil surface, which is stretched cyclically with tidal breathing and this initial mechanical interaction triggers a subsequent cell response. To test this hypothesis, \\e assessed shear stress and strain on the particle-tissue interface and in alveolar \\all Our model consisted of a rigid rod representing an elongated panicle, placed .ti the center of a e\clicall\ stretched extensible disk with physiological compliance (e v. Young modulus of about 25 kPa. and poison ratio of 0.45) representing the al\euliii wall tissue Two possible scenarios for particle-tissue interaction were cvimined. I) contact Traction generated b> cell adhesion molecules (Biophys. J . M oM-gw JW3). ;uul 2) interactions through a thin \iscous la\er The results shi\\cd that the adhesive contact interaction constrained the extension of the tissue surface \\hich resulted in a harp increase of traction along the interface of elongated particle as a Inpeibolic sine function of the distance from the particle -.vnter This indicates that the length ot'deposited fibrous particles pla\s a crucial ji'le in its mechanical interactions on the alveolar wall and that the maximum shear sites- within the alveolar wall occurs at the tips of the particle In the case of a 10 uni înng fibrous panicle, the maximum shear strain could reach as high as 0 5 ( unscquentK, the epithelial cells and connective tissue of the alveolar wall were significant!-, deformed Trie viscous interactions showed more dispersed strain distribution with louer peak value ai ihe tips of the panicle than the ease oi the adhesive interaction, but the peak shear stress (viscous traction on the interface) was substantial[\ higher than the shear stress upicaliy observed on arterial endothelial cell surface We ha\e shown that mechanical damage of the epithelial .c!ls is iikelv to he an important (letJTminant 'n respirator pathoL'cnesis.