Watanabe T, Yamori T
Kansenshogaku Zasshi. 1989 Mar;63(3):182-8. doi: 10.11150/kansenshogakuzasshi1970.63.182.
Primary host defense mechanism of mice against intraperitoneal infection with herpes simplex virus type 1 (HSV-1) was studied using heat-killed Lactobacillus casei YIT 9018 (LC 9018), a bacterial immunostimulant, in combination with inactivated HSV-1 antigen. Peritoneal exudate cells (PECs) in the early period of mice pretreated intraperitoneally (ip) with LC 9018 showed the cytotoxic activity against BALB/3T3 cells infected with HSV-1, in vitro, whereas PECs induced by thioglycollate broth did not. The limitation of HSV-1 replication in monolayers of HSV-1-infected PECs induced by LC 9018 was greater than that in PECs induced by thioglycollate broth. Both activities of PECs induced by LC 9018 were markedly enhanced by the administration of inactivated HSV-1 antigen which showed an interferon-producing activity in the early period after the treatment. These results suggest that the host defense mechanism of mice against intraperitoneal infection with HSV-1 may be mainly related to peritoneal macrophages activated by and interferon produced by the administration of LC 9018 and inactivate HSV-1 antigen.
使用热灭活的干酪乳杆菌YIT 9018（LC 9018）这种细菌免疫刺激剂与灭活的单纯疱疹病毒1型（HSV-1）抗原相结合，研究了小鼠针对HSV-1腹腔感染的主要宿主防御机制。腹腔注射LC 9018预处理的小鼠早期腹腔渗出细胞（PEC）在体外对感染HSV-1的BALB/3T3细胞表现出细胞毒性活性，而由巯基乙酸盐肉汤诱导的PEC则没有。LC 9018诱导的HSV-1感染的PEC单层中HSV-1复制的限制大于巯基乙酸盐肉汤诱导的PEC。LC 9018诱导的PEC的这两种活性通过给予灭活的HSV-1抗原而显著增强，该抗原在治疗后的早期显示出产生干扰素的活性。这些结果表明，小鼠针对HSV-1腹腔感染的宿主防御机制可能主要与由LC 9018和灭活的HSV-1抗原的给药激活的腹腔巨噬细胞和产生的干扰素有关。
