Lactobacillus has been reported to inhibit acute lung injury (ALI). However, the molecular mechanism of Lactobacillus casei (L. casei) in preventing ALI has not been identified, so we investigated whether L. casei pretreatment could inhibit the activation of TLR4/MyD88/NF-κB signaling pathway following ALI. ALI model was established by intraperitoneal injection of 2 mg/kg lipopolysaccharide (LPS) to female BALB/c mice. In L. casei LC2W group, mice were intragastrically administrated L. casei LC2W for a week, before the ALI modeling. The serum of normal BALB/c mice after intragastric administration of L. casei LC2W was used for in vitro cell assays. The serum was pre-incubated with mouse macrophage cell line (RAW264.7) and human lung cell line (HLF-A), then LPS was added to co-incubate. Compared with ALI model group, L. casei LC2W pretreatment significantly reduced lung pathological damage, the number of neutrophils and total cells in bronchoalveolar lavage fluid. Besides, L. casei LC2W pretreatment could significantly reverse the abnormal expression of ICAM-1, IL-6, TNF-α and IL-10 in lung tissue and serum, plus, L. casei LC2W significantly reduced the phosphorylation levels of IRAK-1 and NF-κB p65. In vitro, the serum decreased the up-regulation of IL-6 and TNF-α in cell lines induced by LPS. In conclusion, L. casei LC2W intragastric administration pretreatment could significantly improve LPS-induced ALI in mice, probably through circulation to reach the lungs so as to inhibit the inflammatory response induced by activation of TLR4/MyD88/NF-κB signaling pathway.

据报道，乳酸杆菌可抑制急性肺损伤 (ALI)。然而，干酪乳杆菌（L. casei ）预防 ALI的分子机制尚未确定，因此我们研究了干酪乳杆菌预处理是否可以抑制 ALI 后 TLR4/MyD88/NF-κB 信号通路的激活。向雌性BALB/c小鼠腹腔注射2 mg/kg脂多糖(LPS)建立ALI模型。在干酪乳杆菌LC2W 组中，小鼠被灌胃干酪乳杆菌LC2W一周，ALI建模前。将干酪乳杆菌 LC2W 灌胃后正常 BALB/c 小鼠的血清用于体外细胞测定。将血清与小鼠巨噬细胞系（RAW264.7）和人肺细胞系（HLF-A）预孵育，然后加入LPS共孵育。与ALI模型组相比，L. casei LC2W预处理显着降低了肺病理损伤、支气管肺泡灌洗液中的中性粒细胞数量和总细胞数。此外，L. casei LC2W预处理可显着逆转肺组织和血清中ICAM-1、IL-6、TNF-α和IL-10的异常表达，此外，L. caseiLC2W 显着降低了 IRAK-1 和 NF-κB p65 的磷酸化水平。在体外，血清降低了 LPS 诱导的细胞系中 IL-6 和 TNF-α 的上调。综上所述，干酪乳杆菌LC2W 灌胃预处理可显着改善 LPS 诱导的小鼠 ALI，可能通过循环到达肺部，从而抑制 TLR4/MyD88/NF-κB 信号通路激活诱导的炎症反应。