噬菌体触发抗病毒免疫，防止细菌感染清除。
Bacteriophage trigger antiviral immunity and prevent clearance of bacterial infection.
机构信息
Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University, Stanford, CA, USA.
Stanford Immunology, Stanford University, Stanford, CA, USA.
出版信息
Science. 2019 Mar 29;363(6434). doi: 10.1126/science.aat9691.
Bacteriophage are abundant at sites of bacterial infection, but their effects on mammalian hosts are unclear. We have identified pathogenic roles for filamentous Pf bacteriophage produced by () in suppression of immunity against bacterial infection. Pf promote wound infection in mice and are associated with chronic human wound infections. Murine and human leukocytes endocytose Pf, and internalization of this single-stranded DNA virus results in phage RNA production. This triggers Toll-like receptor 3 (TLR3)- and TIR domain-containing adapter-inducing interferon-β (TRIF)-dependent type I interferon production, inhibition of tumor necrosis factor (TNF), and the suppression of phagocytosis. Conversely, immunization of mice against Pf prevents wound infection. Thus, Pf triggers maladaptive innate viral pattern-recognition responses, which impair bacterial clearance. Vaccination against phage virions represents a potential strategy to prevent bacterial infection.
噬菌体在细菌感染部位大量存在，但它们对哺乳动物宿主的影响尚不清楚。我们已经确定了由 () 产生的丝状 Pf 噬菌体在抑制细菌感染免疫方面的致病作用。Pf 促进小鼠伤口感染，并与慢性人类伤口感染有关。鼠类和人类白细胞内吞 Pf，这种单链 DNA 病毒的内化导致噬菌体 RNA 的产生。这会触发 Toll 样受体 3 (TLR3) 和 TIR 结构域包含衔接子诱导干扰素-β (TRIF) 依赖性 I 型干扰素的产生，抑制肿瘤坏死因子 (TNF)，并抑制吞噬作用。相反，针对 Pf 的小鼠免疫接种可预防伤口感染。因此，Pf 引发适应性先天病毒模式识别反应，从而损害细菌清除。针对噬菌体病毒粒子的疫苗接种代表了预防细菌感染的一种潜在策略。
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