文献类型： 外文期刊

作者： Li, H. Y. ¹ ; Yang, H. G. ³ ; Wu, H. M. ¹ ; Yao, Q. Q. ¹ ; Zhang, Z. Y. ¹ ; Meng, Q. S. ² ; Fan, L. L. ¹ ; Wang, J. Q. ¹ ; Z ¹ ;

作者机构： 1.Chinese Acad Agr Sci, Key Lab Qual & Safety Control Milk & Dairy Prod, Minist Agr & Rural Affairs, Inst Anim Sci, Beijing 100193, Peoples R China

2.Chinese Acad Agr Sci, Inst Anim Sci, Beijing 100193, Peoples R China

3.Minist Agr & Rural Affairs, Key Lab Funct Foods, Sericultural & Agrifood Res Inst, Guangdong Acad Agr Sci, Guangzhou 510610, Peoples R China

关键词： lung inflammation; TLR-4; lactoferrin

期刊名称：JOURNAL OF DAIRY SCIENCE （ 影响因子：4.034； 五年影响因子：4.354 ）

ISSN： 0022-0302

年卷期： 2021 年 104 卷 7 期

页码：

收录情况： SCI

摘要： This study tested the ability of lactoferrin to modu-late pulmonary inflammation. To construct in vitro and in vivo inflammatory lung models, cells from the human lung adenocarcinoma cell line (A549) were exposed to lipopolysaccharide (LPS, 1 & micro;g/mL), and mice (CD-1) were intratracheally administered LPS [10 mg/kg of body weight (BW), tracheal lumen injec-tion], respectively. The A549 cells were preincubated with lactoferrin (10 mg/mL), and the mice were in-traperitoneally injected with lactoferrin (100 mg/kg of BW), followed by LPS treatment. The concentrations of proinflammatory cytokines (IL-1 beta and TNF-alpha) in culture medium of A549 cells and in bronchoalveolar lavage fluid of the mice were determined using enzyme-linked immunosorbent assays. The toll-like receptor 4-related pathway (TLR4/MyD88/IRAK1/TRAF6/ NF kappa B) was determined at gene and protein expression levels in A549 cells and mouse lung tissue. Results showed that LPS treatment significantly elevated the concentrations of IL-1 beta and TNF-alpha in the A549 cell culture medium and in bronchoalveolar lavage fluid of the mice; it also elevated both the mRNA and protein expressions of TLR4 and the TLR4 downstream factors in A549 cells and mouse lung tissue. Nevertheless, lac-toferrin apparently depressed the releases of IL-1 beta and TNF-alpha from A549 cells and lung tissues stimulated by LPS, and significantly suppressed the TLR4 signaling pathway. Lactoferrin also promoted the enhancement of miR-146a expression in A549 cells and mouse lung tissue. Moreover, 100 degrees C heating for 3 min caused total loss of the previously listed bioactivity of lactoferrin. Collectively, we proved that lactoferrin intervened inLPS-induced inflammation in the pulmonary cell model and in the mouse model, through inhibiting the TLR4- related pathway.