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.

中文翻译：

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白细胞介素1β和脂多糖诱导决定软骨细胞形态特性并相对降低细胞粗糙度和粘附能

骨关节炎（OA）是一种以关节软骨（AC）组织退化、慢性炎症和骨重塑为特征的全关节疾病。AC 损伤后，包括白细胞介素 1β (IL1β) 和脂多糖 (LPS) 在内的促炎介质在 OA 的发生和进展中发挥着重要作用。本研究的目的是从机械角度检测并比较 IL1β 和 LPS 分别对牛软骨细胞形态和纳米力学特性的影响。将细胞在全血清培养基中接种过夜，第二天分为三个主要组：低血清培养基的阴性对照 (NC) 和 10 ng/ml IL1ß 或 10 ng/ml LPS 修饰培养基。诱导细胞24小时。使用原子力显微镜量化纳米机械性能（弹性模量和粘附能）和粗糙度。一氧化氮、前列腺素 2 (PGE2) 和基质金属蛋白酶 3 (MMP3) 含量；细胞活力；并对细胞外基质成分进行定量。我们的数据显示，细胞的活力不受炎症诱导的影响，并且 IL1ß 诱导增加了 PGE2。IL1β和NC之间的细胞弹性模量相似，而LPS与NC相比显着降低了弹性。与 NC 相比，IL1ß 诱导导致细胞粗糙度最小，而 LPS 诱导导致粘附能最小。我们的图像表明 IL1ß 和 LPS 炎症通过细胞骨架重排和应力纤维的存在影响细胞形态。最后，我们的结果表明，两种研究的炎症介质以不同的方式调节软骨细胞对炎症的立即反应。