Bacterial infection is one of the main causes of bovine respiratory disease (BRD), which can cause tremendous losses for the herd farming industry worldwide. l-Glutamine (GLN), a neutral amino acid, has been reported to have anti-inflammatory properties. This study aims to explore the potential protective effects and mechanisms of GLN on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. Forty ICR mice were randomly divided into four groups (n = 10): a PBS intratracheal instillation group, a LPS intratracheal instillation group, a GLN gavage group, and a LPS+GLN group (GLN was given 1 h before the LPS stimulation). Twelve hours after LPS administration, the lung tissue and blood were collected. The results showed that the concentrations of IL-6, IL-8, and IL-1β; the protein abundance of the toll-like receptor 4 (TLR4), phosphorylated p38 (p-p38), phosphorylated ERK1/2 (p-ERK1/2), and phosphorylated JNK (p-JNK); and the expression level of genes associated with inflammation, such as IL-1β, IL-8, TNF-α, IL-6, TLR4, p38, ERK1/2, and JNK, were significantly increased in the LPS group compared with those in the PBS group. However, these increases were attenuated by GLN pretreatment in the LPS+GLN group. Furthermore, the pathological change of the structure of lung tissue from the LPS group was obvious compared to that from the PBS group; however, with GLN administration, these pathological changes were alleviated. Additionally, the secretion level of mucus and the percentage of positive MUC5AC staining on the epithelial surface area of the airway increased dramatically in the LPS group; however, GLN pretreatment in the LPS+GLN group markedly decreased these phenomena compared with that of the LPS group. These results indicate that GLN supplementation ameliorates LPS-induced ALI in mice and this effect may be mediated by the TLR4/MAPK signaling pathway.

细菌感染是牛呼吸道疾病（BRD）的主要原因之一，会给全球畜牧业造成巨大损失。 l-谷氨酰胺 (GLN) 是一种中性氨基酸，据报道具有抗炎特性。本研究旨在探讨GLN对脂多糖（LPS）诱导的小鼠急性肺损伤（ALI）的潜在保护作用和机制。将 40 只 ICR 小鼠随机分为 4 组（n = 10）：PBS 气管内滴注组、LPS 气管内滴注组、GLN 灌胃组、LPS+GLN 组（GLN 在 LPS 刺激前 1 h 给予）。 LPS施用12小时后，收集肺组织和血液。结果显示，IL-6、IL-8、IL-1β的浓度； Toll 样受体 4 (TLR4)、磷酸化 p38 (p-p38)、磷酸化 ERK1/2 (p-ERK1/2) 和磷酸化 JNK (p-JNK) 的蛋白质丰度； LPS组与炎症相关的基因IL-1β、IL-8、TNF-α、IL-6、TLR4、p38、ERK1/2、JNK等表达量较对照组显着升高。美国公共广播公司（PBS）小组。然而，LPS+GLN 组中的 GLN 预处理减弱了这些增加。此外，LPS组肺组织结构病理改变较PBS组明显；然而，使用 GLN 后，这些病理变化得到缓解。此外，LPS组的粘液分泌水平和气道上皮表面MUC5AC染色阳性的百分比显着增加；然而，与LPS组相比，LPS+GLN组的GLN预处理显着减少了这些现象。 这些结果表明，补充 GLN 可改善 LPS 诱导的小鼠 ALI，这种作用可能是由 TLR4/MAPK 信号通路介导的。