Interleukin 1β and lipopolysaccharides induction dictate chondrocyte morphological properties and reduce cellular roughness and adhesion energy comparatively

Osteoarthritis (OA) is a whole joint disease marked by the degradation of the articular cartilage (AC) tissue, chronic inflammation, and bone remodeling. Upon AC’s injury, proinflammatory mediators including interleukin 1β (IL1β) and lipopolysaccharides (LPS) play major roles in the onset and progression of OA. The objective of this study was to mechanistically detect and compare the effects of IL1β and LPS, separately, on the morphological and nanomechanical properties of bovine chondrocytes. Cells were seeded overnight in a full serum medium and the next day divided into three main groups: A negative control (NC) of a reduced serum medium and 10 ng/ml IL1ß or 10 ng/ml LPS-modified media. Cells were induced for 24 h. Nanomechanical properties (elastic modulus and adhesion energy) and roughness were quantified using atomic force microscopy. Nitric oxide, prostaglandin 2 (PGE2), and matrix metalloproteinases 3 (MMP3) contents; viability of cells; and extracellular matrix components were quantified. Our data revealed that viability of the cells was not affected by inflammatory induction and IL1ß induction increased PGE2. Elastic moduli of cells were similar among IL1β and NC while LPS significantly decreased the elasticity compared to NC. IL1ß induction resulted in least cellular roughness while LPS induction resulted in least adhesion energy compared to NC. Our images suggest that IL1ß and LPS inflammation affect cellular morphology with cytoskeleton rearrangements and the presence of stress fibers. Finally, our results suggest that the two investigated inflammatory mediators modulated chondrocytes’ immediate responses to inflammation in variable ways.