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首页> 美国卫生研究院文献>Infection and Immunity >Stimulation of gp91 Phagocytic Oxidase and Reactive Oxygen Species in Neutrophils by an Avirulent Salmonella enterica Serovar Infantis Strain Protects Gnotobiotic Piglets from Lethal Challenge with Serovar Typhimurium Strain F98 without Inducing Intestinal Pathology
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Stimulation of gp91 Phagocytic Oxidase and Reactive Oxygen Species in Neutrophils by an Avirulent Salmonella enterica Serovar Infantis Strain Protects Gnotobiotic Piglets from Lethal Challenge with Serovar Typhimurium Strain F98 without Inducing Intestinal Pathology

机译：无毒肠炎沙门氏菌Sfanvar Infantis菌株刺激中性粒细胞中的gp91吞噬性氧化酶和反应性氧物种通过血清型鼠伤寒F98菌株保护Gnotobiotic小猪免受致死性攻击而不会引起肠道病理学改变。

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Preinoculation of susceptible 5-day-old gnotobiotic piglets with Salmonella enterica serovar Infantis strain 1326/28Φr stimulates neutrophil migration into the intestine, which rapidly protects the pigs against a subsequent (normally lethal) challenge with S. enterica serovar Typhimurium strain F98. Here we show that inoculation with either 1326/28Φr or F98 activated reactive oxygen species (ROS) in neutrophils via NADPH pathways in vivo and in vitro and that the survival of both Salmonella strains was increased if neutrophils were cocultured with the ROS inhibitor N-acetylcysteine (captopril). Neither F98 nor 1326/28Φr significantly increased reactive nitrogen species (RNS) levels in neutrophils isolated from uninfected pigs. Our results indicate the following: (i) rapid protection of highly susceptible gnotobiotic piglets against F98-induced gastroenteritis by preinoculation with 1326/28Φr is likely to be due to stimulation of ROS-producing neutrophils in the intestinal epithelium prior to challenge with the lethal strain; (ii) pathological lesions of the intestine during severe gastroenteritis are not necessarily induced by neutrophil migration per se; and (iii) if neutrophil migration into the intestine is responsible for pathology, then neither increased production of ROS or RNS (in pigs inoculated with the lethal strain) nor reduced production (in protected pigs in which pathological lesions are ameliorated by preinoculation with 1326/28Φr) can account for this phenomenon.
机译：对易感的5天大的致生性仔猪预先接种肠炎沙门氏菌Infantis毒株1326 /28Φ r 会刺激嗜中性粒细胞迁移到肠道，从而迅速保护猪免受随后的S攻击（通常是致命的）。肠球菌鼠伤寒菌株F98。在这里，我们显示了通过NADPH途径体内和体外接种中性粒细胞的1326 /28Φ r 或F98活化的活性氧（ROS），并且如果中性粒细胞被感染，两种沙门氏菌菌株的存活率都会增加。与ROS抑制剂N-乙酰半胱氨酸（卡托普利）共培养。 F98和1326 /28Φ r 均未显着增加从未感染猪中分离出的中性粒细胞的反应性氮物种（RNS）水平。我们的结果表明：（i）通过预先接种1326 /28Φ r 来快速保护高度易感的致生性仔猪免受F98诱导的胃肠炎的侵袭，可能是由于刺激了肠道中产生ROS的中性粒细胞的刺激所致。致死菌株攻击前上皮; （ii）嗜中性粒细胞迁移本身不一定导致严重胃肠炎期间肠道的病理损害； （iii）如果中性粒细胞迁移到肠道是造成病理的原因，则既不增加ROS或RNS的产量（在接种了致命株的猪中），也不减少产量（在受保护的猪中，预先接种1326 /可以减轻病理损伤） 28Φ r ）可以解释这种现象。

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