Oncotarget

Research Papers:

Lipocalin 2 regulates intestine bacterial survival by interplaying with siderophore in a weaned piglet model of Escherichia coli infection

Bing-Xiu Guo, Qian-Qian Wang, Jia-Hui Li, Zhen-Shun Gan, Xiao-Feng Zhang, Yi-Zhen Wang and Hua-Hua Du _

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Oncotarget. 2017; 8:65386-65396. https://doi.org/10.18632/oncotarget.18528

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Abstract

Bing-Xiu Guo1, Qian-Qian Wang1,2, Jia-Hui Li1,2, Zhen-Shun Gan1, Xiao-Feng Zhang3, Yi-Zhen Wang1,2 and Hua-Hua Du1,2

1College of Animal Science, Zhejiang University, Hangzhou, 310058, China

2Key Laboratory of Animal Nutrition and Feed Science, Eastern of China, Ministry of Agriculture, Zhejiang University, Hangzhou, 310058, China

3Institute of Animal Husbandry and Veterinary Science, Zhejiang Academy of Agricultural Sciences, Hangzhou, 310021, China

Correspondence to:

Hua-Hua Du, email: huahuadu@zju.edu.cn

Keywords: lipocalin 2, siderophore, Escherichia coli K88, iron sequestration, intestinal infection

Received: May 10, 2017     Accepted: June 05, 2017     Published: June 16, 2017

ABSTRACT

Iron is an essential nutrient that facilitates cell proliferation and growth, which plays a pivotal role in modulating the battle for survival between mammalian hosts and their pathogens. Pathogenic bacteria secrete siderophores to acquire iron from the host. However, lipocalin 2 (Lcn2), a siderophore-binding antimicrobial protein, binds to siderophores to prevent bacterial uptake of iron, which is critical for the control of systemic infection with Escherichia coli (E. coli). But few studies focus on the anti-infective response of Lcn2 in the intestines by inhibiting bacterial proliferation based on microbial iron metabolism. In this study, we showed that iron was sequestrated within cells in a piglet model of E. coli K88 infection. Siderophores was produced following E. coli K88 infection and siderophore-related genes expression was upregulated in iron-deficiency environment in vitro. Meanwhile, we found that Lcn2 expression was rapidly and robustly induced in jejunum by E. coli K88 infection and could be stimulated by IL-17 and IL-22. Furthermore, both Lcn2 induced in epithelial cells IPEC-1 and added exogenously as a recombinant protein could inhibit the growth of E. coli. We can conclude that Lcn2 is a crucial component of mucosal immune defense against intestinal infection with E. coli K88.


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