Iron is an essential nutrient for bacterial growth. Therefore, bacteria have evolved chelation mechanisms to acquire iron for their survival. Enterobactin, a chelator with high affinity for ferric iron, is secreted by Escherichia coli and contributes to its improved bacterial fitness. In this preliminary study, we evaluated enterobactin deficiency both in vitro and in vivo in the context of E. coli mastitis. Firstly, we showed that expression of lipocalin 2, a protein produced by the host that is able to both bind and deplete enterobactin, is increased upon E. coli infection in the cow's mastitic mammary gland. Secondly, we demonstrated in vitro that enterobactin deficiency does not alter interleukin (IL)-8 expression in bovine mammary epithelial cells and its associated neutrophil recruitment. However, a significantly increased reactive oxygen species production of these neutrophils was observed. Thirdly, we showed there was no significant difference in bacterial in vitro growth between the enterobactin-deficient mutant and its wild-type counterpart. However, when further explored in a murine model for bovine mastitis, the enterobactin-deficient mutant vs. the wild-type strain revealed a significant reduction of the bacterial load and, consequently, a decrease in pro-inflammatory cytokines (IL-1α,−1β,−4,−6, and−8). A reduced neutrophilic influx was also observed immunohistochemically. These findings therefore identify interference of the enterobactin iron-scavenging mechanism as a potential measure to decrease the fitness of E. coli in the mastitic mammary gland.

铁是细菌生长的必需营养素。因此，细菌进化出了螯合机制来获取铁以维持其生存。肠杆菌素是一种对三价铁具有高亲和力的螯合剂，由大肠杆菌并有助于改善细菌适应性。在这项初步研究中，我们评估了肠杆菌素缺乏症体外和体内在这样的背景下大肠杆菌乳腺炎。首先，我们发现脂质运载蛋白 2 的表达增加，脂质运载蛋白 2 是一种由宿主产生的蛋白质，能够结合并消耗肠杆菌素。大肠杆菌奶牛乳腺感染。其次，我们展示了体外肠杆菌素缺乏不会改变牛乳腺上皮细胞中白细胞介素 (IL)-8 的表达及其相关的中性粒细胞募集。然而，观察到这些嗜中性粒细胞的活性氧产生显着增加。第三，我们发现细菌没有显着差异。体外肠杆菌素缺陷型突变体与其野生型对应物之间的生长。然而，当在牛乳腺炎小鼠模型中进一步探索时，与野生型菌株相比，肠杆菌素缺陷突变体显示细菌负荷显着减少，因此促炎细胞因子（IL-1α，− 1β,−4,−6,−8)。免疫组织化学还观察到中性粒细胞流入减少。因此，这些发现将肠杆菌素铁清除机制的干扰确定为降低铁的适应性的潜在措施。大肠杆菌在乳腺中。