Preconditioning with Lipopolysaccharide or Lipoteichoic Acid Protects against Staphylococcus aureus Mammary Infection in Mice.
Preconditioning with Lipopolysaccharide or Lipoteichoic Acid Protects against Staphylococcus aureus Mammary Infection in Mice.
复制标题
用脂多糖或脂肪酸的预处理可防止小鼠葡萄球菌乳腺乳腺感染。
DOI：
10.3389/fimmu.2017.00833
复制
发表时间：
2017
影响因子：
7.3
通讯作者：
Meyer E
中科院分区：
文献类型：
--
作者：
Breyne K;Steenbrugge J;Demeyere K;Vanden Berghe T;Meyer E
金黄色葡萄球菌是乳腺炎的最主要病原体之一，与慢性乳房感染有关。病原体的持续存在被认为是局部炎症信号传导触发不足的结果。在这项研究中，使用临床前乳腺炎模型，旨在评估脂多糖（LPS）或脂磷壁酸（LTA）预处理是否可以帮助宿主更有效地清除或至少限制随后的S。金黄色葡萄球菌感染。原型革兰氏阴性毒力因子，即，LPS和革兰氏阳性毒力因子，即筛选LTA是否能够增强局部免疫区室。相比S。金黄色葡萄球菌诱导的炎症中，两种毒素都具有显著的高效力以有效诱导两种新的选择的先天免疫生物标志物，脂质运载蛋白2（LCN 2）和几丁质酶3样1（CHI 3L 1）。当在局部S.金黄色葡萄球菌感染后，我们能够调节先天免疫应答，减少局部细菌负荷，并在感染后24小时诱导LCN 2或CHI 3L 1。对乳腺巨噬细胞的氯膦酸盐消耗也发现，巨噬细胞对S.金黄色葡萄球菌感染。基于组织学中性粒细胞内流评价、伴随的局部细胞因子谱和LCN 2/CHI 3L 1模式，巨噬细胞非依赖性信号传导在LPS或LTA预处理的S.金黄色葡萄球菌感染的小鼠乳腺。我们的研究结果强调了在乳腺先天免疫反应过程中警惕微环境的重要性，并为有效免疫调节局部细菌感染的新方法提供了新的见解。
Staphylococcus aureus is one of the most causative agents of mastitis and is associated with chronic udder infections. The persistency of the pathogen is believed to be the result of an insufficient triggering of local inflammatory signaling. In this study, the preclinical mastitis model was used, aiming to evaluate if lipopolysaccharide (LPS) or lipoteichoic acid (LTA) preconditioning could aid the host in more effectively clearing or at least limiting a subsequent S. aureus infection. A prototypic Gram-negative virulence factor, i.e., LPS and Gram-positive virulence factor, i.e., LTA were screened whether they were able to boost the local immune compartment. Compared to S. aureus-induced inflammation, both toxins had a remarkable high potency to efficiently induce two novel selected innate immunity biomarkers i.e., lipocalin 2 (LCN2) and chitinase 3-like 1 (CHI3L1). When combining mammary inoculation of LPS or LTA prior to a local S. aureus infection, we were able to modulate the innate immune response, reduce local bacterial loads, and induce either LCN2 or CHI3L1 at 24 h post-infection. Clodronate depletion of mammary macrophages also identified that macrophages contribute only to a limited extend to the LPS/LTA-induced immunomodulation upon S. aureus infection. Based on histological neutrophil influx evaluation, concomitant local cytokine profiles and LCN2/CHI3L1 patterns, the macrophage-independent signaling plays a major role in the LPS- or LTA-pretreated S. aureus-infected mouse mammary gland. Our results highlight the importance of a vigilant microenvironment during the innate immune response of the mammary gland and offer novel insights for new approaches concerning effective immunomodulation against a local bacterial infection.