The purpose of the current study was to explore the effect of autologous adipose tissue on cartilage responses to lipopolysaccharide (LPS). We hypothesized that LPS elicits an inflammatory response in cartilage, and that response is augmented in the presence of adipose tissue. Furthermore, we hypothesized that this augmented inflammatory response is due, at least in part, to increased exposure of cartilage to adipose tissue-derived c3a. Porcine cartilage explants from market-weight pigs were cultured in the presence or absence of autologous adipose tissue for 96 hours, the final 48 hours of which they were stimulated with LPS (0 or 10 μg/mL). Adipose tissue explants were also cultured alone, in the presence or absence of LPS. Media from all cartilage treatments was assayed for c3a/c3a des Arg, PGE₂, GAG, and NO, and the viability of cartilage tissue was determined by differential fluorescent staining. Media from adipose tissue explants was assayed for c3a/c3a des Arg and PGE₂. LPS produced a significant increase in PGE₂, GAG, and NO production when cartilage was cultured in the absence of adipose tissue. Coculture of adipose tissue prevented a significant increase in PGE₂ in cartilage explants. There was no effect of adipose tissue on LPS-induced GAG or NO, but the presence of adipose tissue significantly reduced cell viability in LPS-stimulated cartilage explants. Adipose tissue explants from lean animals reduced inflammatory responses of cartilage to LPS via a c3a/c3a des Arg-independent mechanism and were associated with a significant decline in cell viability. Thus, contrary to our hypothesis, adipose tissue from lean animals does not augment the inflammatory response of cartilage to stimulation by LPS. The mechanism of modulatory effects of adipose tissue on LPS-induced increase in PGE₂ and decline in chondrocyte viability requires further research but appears to have occurred via a mechanism that is independent of adipocentric c3a/c3a des Arg.

中文翻译：

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在自体脂肪组织存在下培养关节软骨外植体改变它们对脂多糖的炎症反应

本研究的目的是探讨自体脂肪组织对脂多糖 (LPS) 软骨反应的影响。我们假设 LPS 在软骨中引发炎症反应，并且在脂肪组织存在的情况下，这种反应会增强。此外，我们假设这种增强的炎症反应至少部分是由于软骨暴露于脂肪组织来源的 c3a 增加。来自市场体重猪的猪软骨外植体在存在或不存在自体脂肪组织的情况下培养 96 小时，最后 48 小时用 LPS（0 或 10 μg /mL）刺激 。在存在或不存在 LPS 的情况下，脂肪组织外植体也单独培养。测定来自所有软骨处理的培养基的 c3a/c3a des Arg、PGE₂、GAG和NO，以及软骨组织的活力通过差示荧光染色确定。对来自脂肪组织外植体的培养基测定 c3a/c3a des Arg 和 PGE ₂。当在没有脂肪组织的情况下培养软骨时，LPS 使 PGE ₂、GAG 和 NO 的产生显着增加。脂肪组织的共培养阻止了 PGE ₂的显着增加在软骨外植体中。脂肪组织对 LPS 诱导的 GAG 或 NO 没有影响，但脂肪组织的存在显着降低了 LPS 刺激的软骨外植体中的细胞活力。来自瘦动物的脂肪组织外植体通过 c3a/c3a des Arg 独立机制降低了软骨对 LPS 的炎症反应，并且与细胞活力的显着下降有关。因此，与我们的假设相反，瘦动物的脂肪组织不会增强软骨对 LPS 刺激的炎症反应。脂肪组织对 LPS 诱导的 PGE ₂增加和软骨细胞活力下降的调节作用机制需要进一步研究，但似乎是通过独立于脂肪中心 c3a/c3a des Arg 的机制发生的。