Lipopolysaccharide and lipoteichoic acid enhance serum amyloid A3 mRNA expression in murine alveolar epithelial cells

被引:5
|
作者
Iwata, Ami [1 ]
Shimizu, Kaori [1 ]
Kawasaki, Haruka [1 ]
Okada, Ayaka [1 ,2 ]
Inoshima, Yasuo [1 ,2 ,3 ,4 ]
机构
[1] Gifu Univ, Cooperat Dept Vet Med, Lab Food & Environm Hyg, Gifu 5011193, Japan
[2] Gifu Univ GeFAH, Educ & Res Ctr Food Anim Hlth, Gifu 5011193, Japan
[3] Gifu Univ, United Grad Sch Vet Sci, Gifu 5011193, Japan
[4] Gifu Univ, Joint Grad Sch Vet Sci, Gifu 5011193, Japan
来源
JOURNAL OF VETERINARY MEDICAL SCIENCE | 2019年 / 81卷 / 10期
关键词
epithelium; innate immunity; lung; serum amyloid A; serum amyloid A3; SURFACTANT; RECEPTORS; PROTEIN; GROWTH;
D O I
10.1292/jvms.19-0154
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Serum amyloid A (SAA) is an acute-phase protein indicative of inflammation. In murine colonic epithelial cells, lipopolysaccharide (LPS), a gram-negative bacterial antigen, strongly enhanced mRNA expression of SAA3, but not SAA1 or SAA2, suggesting that SAA3 might respond to bacterial infection in other epithelia. We examined SAA1/2 and SAA3 mRNA expression in murine alveolar epithelial cells exposed to LPS or the gram-positive bacterial antigen, lipoteichoic acid (LTA), using real-time PCR. LPS enhanced SAA3 mRNA expression at lower concentrations than did LTA, whereas SAA1/2 mRNA expression was not enhanced by either LPS or LTA. These results suggest that SAA3 expression is enhanced in lung epithelium upon bacterial infection as part of innate immunity, with higher sensitivity to LPS than to LTA.
引用
收藏
页码:1409 / 1412
页数:4
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