Influenza A viruses upregulate neutrophil toll-like receptor 2 expression and function
Influenza A viruses upregulate neutrophil toll-like receptor 2 expression and function
复制标题
DOI：
10.1111/j.1365-3083.2005.01714.x
复制
发表时间：
2006-02-01
影响因子：
3.7
通讯作者：
Hartshorn, KL
中科院分区：
文献类型：
--
作者：
Lee, RM;White, MR;Hartshorn, KL
中性粒细胞参与对甲型流感病毒（IAV）感染的初始宿主反应，并在暴露于病毒后表现出激活和抑制功能。我们证明IAV引起中性粒细胞toll样受体2 （TLR2）表达的快速上调。中性粒细胞激动剂甲酰基甲基多酰丙氨酸（fMLP）、C5a和脂多糖不改变中性粒细胞TLR2的表达，而PMA和微生物TLR2配体肽聚糖（PGN）和酶san降低了中性粒细胞TLR2的表达。为了确定iav诱导的TLR2表达增加的功能意义，我们将iav处理的中性粒细胞暴露于PGN、金黄色葡萄球菌（S. aureus）和zymosan。IAV预处理可显著增加金黄色葡萄球菌和酵素的摄取，并加速中性粒细胞凋亡。iav处理的细胞对PGN产生了更多的H2O2。这些结果表明，IAV增加了中性粒细胞表面TLR2的表达，并调节了对结合TLR2的配体的功能反应。这些发现可能阐明iav诱导的中性粒细胞功能在体内的扰动。
Neutrophils are involved in the initial host response to influenza A virus (IAV) infection and exhibit both activation and depressed function after exposure to the virus. We demonstrate that IAV causes rapid upregulation of Toll-like receptor 2 (TLR2) expression on neutrophils. The neutrophil agonists, formyl-methylpleucyl-alanine (fMLP), C5a and lipopolysaccharide did not alter neutrophil TLR2 expression, whereas PMA and the microbial TLR2 ligands, peptidoglycan (PGN) and zymosan, reduced it. To determine the functional significance of IAV-induced increase in TLR2 expression, IAV-treated neutrophils were exposed to PGN, Staphylococcus aureus (S. aureus) and zymosan. Pretreatment with IAV resulted in significantly increased uptake of S. aureus and zymosan and accelerated neutrophil apoptosis when combined with S. aureus. IAV-treated cells generated significantly more H2O2 in response to PGN. These results indicate that IAV increases neutrophil surface expression of TLR2 and modulates functional responses to ligands that bind TLR2. These findings may clarify IAV-induced perturbation of neutrophil functions in vivo.