Data on importance of hematopoietic cell derived Lipocalin 2 against gut inflammation

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• 作者：Piu Saha^a ; Vishal Singh^a ; Xia Xiao^a ; Beng San Yeoh^a ; Matam Vijay-Kumar^a ; ^b ; ^{mvk13@psu.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Siderocalin ; Gut microbiota ; Inflammatory bowel disease ; Bone marrow chimeras ; Colitis
• 刊名：Data in Brief
• 出版年：2016
• 出版时间：September 2016
• 年：2016
• 卷：8
• 期：Complete
• 页码：812-816
• 全文大小：1136 K

文摘

The data herein is related to the research article entitled “Microbiota-inducible innate immune siderophore binding protein Lipocalin 2 is critical for intestinal homeostasis” (Singh et al., 2016) [1]. In the present article, we monitored dextran sodium sulfate (DSS)-induced colitis development upon Lipocalin 2 (Lcn2) neutralization, and examined the survival of Lcn2 deficient (Lcn2KO) mice and their WT littermates upon DSS challenge. To dissect the relative contribution of immune and non-immune cells-derived Lcn2 in mediating protection against gut inflammation, we generated respective bone marrow chimera and evaluated their susceptibility to IL-10 receptor neutralization-induced chronic colitis.

Neutralization of Lcn2 in WT mice resulted in exacerbated DSS-induced colitis. Notably, mice lacking Lcn2 exhibited 100% mortality whereas only 20% mortality was observed in WT mice upon DSS challenge. Further, data from bone marrow chimera showed that immune cell-derived Lcn2 is the major contributor in conferring protection against colitis.