Probiotics are known to modulate gut microbiota, intestinal barrier function and host immune response, but due to the species and strain specific response their mechanisms are not clearly understood. Thus, the present study was designed to isolate, assess the anti-inflammatory potential and underlying modulatory mechanisms of indigenous probiotics in murine macrophage cell line, RAW 264.7. Forty lactic acid bacteria (LAB) were isolated from different sources and monitored for their anti-inflammatory potential against lipopolysaccharide (LPS) induced inflammatory stress employing RAW 264.7 cells. Among these isolates, only four LAB isolates exhibited more than 90% nitric oxide inhibition and possessed the probiotic attributes. Further, these selected LAB isolates reduced the level of pro-inflammatory cytokines, TNF-α, IL-1β and IL-6, inhibited the phosphorylation of Mitogen Activated Protein Kinases (MAPKs) i.e. p38 MAPK, ERK1/2 and SAPK/JNK and expression of cyclooxygenase-2 (COX-2) in LPS stimulated RAW 264.7 cells. The in vitro analysis suggested that the selected probiotic isolates attenuated the LPS-induced inflammation by downregulating MAPK pathway vis-a-vis inhibiting COX-2 and can be employed as anti-inflammatory agents in various inflammatory diseases.

中文翻译：

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脂多糖刺激的 RAW 264.7 巨噬细胞中益生菌的分离、表征和抗炎机制

已知益生菌可调节肠道微生物群、肠道屏障功能和宿主免疫反应，但由于物种和菌株的特异性反应，它们的机制尚不清楚。因此，本研究旨在分离、评估鼠巨噬细胞系 RAW 264.7 中土著益生菌的抗炎潜力和潜在调节机制。从不同来源中分离出 40 种乳酸菌 (LAB)，并使用 RAW 264.7 细胞监测它们对脂多糖 (LPS) 诱导的炎症应激的抗炎潜力。在这些分离株中，只有 4 个 LAB 分离株表现出超过 90% 的一氧化氮抑制并具有益生菌属性。此外，这些选定的 LAB 分离株降低了促炎细胞因子、TNF-α、IL-1β 和 IL-6 的水平，在 LPS 刺激的 RAW 264.7 细胞中抑制丝裂原活化蛋白激酶 (MAPK) 即 p38 MAPK、ERK1/2 和 SAPK/JNK 的磷酸化以及环氧合酶-2 (COX-2) 的表达。体外分析表明，选定的益生菌分离物通过下调 MAPK 通路与抑制 COX-2 来减轻 LPS 诱导的炎症，并可用作各种炎症疾病的抗炎剂。