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] where we have demonstrated that C57BL/6 Lipocalin 2 deficient mice (Lcn2KO) developed chronic colitis upon anti-interleukin-10 receptor (αIL-10R) monoclonal antibody administration. In the present article, we evaluated the susceptibility of BALB/c Lcn2KO mice and their WT littermates to the αIL-10R neutralization-induced chronic colitis. Our data showed that αIL-10R mAb-treated BALB/c Lcn2KO mice exhibited severe chronic colitis (i.e., splenomegaly, colomegaly, colonic pathology, and incidence of rectal prolapse) when compared to WT mice.This article is published as Singh, Vishal, Beng San Yeoh, Marit Nilsen-Hamilton, Thorsten Berger, Tak W. Mak, and Matam Vijay-Kumar. "Data on IL-10R neutralization-induced chronic colitis in Lipocalin 2 deficient mice on BALB/c background." Data in brief 11 (2017): 588-592. doi: 10.1016/j.dib.2017.03.002.</p

Berger, Thorsten

Mak, Tak

Nilsen-Hamilton, Marit

Singh, Vishal

Vijay-Kumar, Matam

Yeoh, Beng San

Digital Repository @ Iowa State University (ISU)

Contents lists available at ScienceDirectData in BriefData in Brief 11 (2017) 588–592Shttp://d2352-34(http://cDOIn CorrUniversE-mjournal homepage: www.elsevier.com/locate/dibData ArticleData on IL-10R neutralization-induced chroniccolitis in Lipocalin 2 deficient mice onBALB/c backgroundVishal Singh a, Beng San Yeoh a, Marit Nilsen-Hamilton b,Thorsten Berger c, Tak W. Mak c, Matam Vijay-Kumar a,na Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 16802, USAb Department of Biochemistry, Biophysics and Molecular Biology, Iowa State University, Ames, IA 50011, USAc The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, CanadaM5G 2C1a r t i c l e i n f oArticle history:Received 7 February 2017Received in revised form1 March 2017Accepted 3 March 2017Available online 8 March 2017Keywords:SiderocalinNeutrophil gelatinase-associated lipocalinInflammatory bowel diseaseIL-10x.doi.org/10.1016/j.dib.2017.03.00209/& 2017 The Authors. Published by Elsevreativecommons.org/licenses/by/4.0/).of original article: http://dx.doi.org/10.1016espondence to: Department of Nutritionaity Park, PA 16802, USA. Fax: þ1 814 863 6ail address: mvk13@psu.edu (M. Vijay-Kuma b s t r a c tThe data herein is related to the research article entitled “Micro-biota-inducible Innate Immune, Siderophore Binding ProteinLipocalin 2 is Critical for Intestinal Homeostasis” (Singh et al.,2016) [1] where we have demonstrated that C57BL/6 Lipocalin2 deficient mice (Lcn2KO) developed chronic colitis upon anti-interleukin-10 receptor (αIL-10R) monoclonal antibody adminis-tration. In the present article, we evaluated the susceptibility ofBALB/c Lcn2KO mice and their WT littermates to the αIL-10Rneutralization-induced chronic colitis. Our data showed that αIL-10R mAb-treated BALB/c Lcn2KO mice exhibited severe chroniccolitis (i.e., splenomegaly, colomegaly, colonic pathology, andincidence of rectal prolapse) when compared to WT mice.& 2017 The Authors. Published by Elsevier Inc. This is an openaccess article under the CC BY license(http://creativecommons.org/licenses/by/4.0/).Specifications Tableubject area BiologyLipocalin 2, inflammatory bowel diseaseier Inc. This is an open access article under the CC BY license/j.jcmgh.2016.03.007l Sciences, The Pennsylvania State University, 222 Chandlee Laboratory,103.ar).MTHDEEDV. Singh et al. / Data in Brief 11 (2017) 588–592 589ore specific sub-ject areaype of data Graphs, images, figuresow data wasacquiredAssessment of colitis parameters: splenomegaly, colomegaly, colon histology,enzyme-linked immunosorbent assay (ELISA), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Biotek Eon™ microplatespectrophotometer and Step One Plus Real-Time PCR System.ata format AnalyzedxperimentalfactorsLcn2KO mice and their WT littermates were treated with anti-IL-10R mono-clonal antibody or anti-IgG isotype control as described in Ref. [1]xperimentalfeaturesAnalysis of standard colitis parametersata sourcelocationPennsylvania, USAata accessibility Data are provided with this articleDValue of the data The data are valuable to researchers interested in investigating the role of lipocalin 2 (Lcn2) ininflammatory bowel disease. The data indicate that Lcn2 deficiency predisposes to colitis and this phenotype can be recapitu-lated in mice on the BALB/c background. The data support future studies in delineating the role of Lcn2 in conferring mucoprotection.1. DataThe dataset of this article provides additional information to Ref. [1], in which we have char-acterized the increased susceptibility of C57BL/6 lipocalin 2 knockout (Lcn2KO) mice to colitis. Con-sidering that the mouse genetic background can influence colitogenesis [i.e., immune responses ofC57BL/6 and BALB/c mice are Th1 and Th2-biased, respectively [2–5], we herein investigated thesusceptibility of BALB/c Lcn2KO mice to interleukin-10 receptor (IL-10R) neutralization-inducedchronic colitis. The data presented here elucidate that the robust chronic colitis observed in αIL-10R-treated C57BL/6 Lcn2KO mice [1] can be recapitulated in BALB/c Lcn2KO mice. Specifically,splenomegaly, colomegaly, and elevated serum and colonic inflammation markers were observed inαIL-10R-treated BALB/c Lcn2KO mice when compared to their respective WT control (Fig. 1A–E).Remarkably, BALB/c Lcn2KO mice exhibited rectal prolapse, a severe form of colitis, upon IL-10Rneutralization (Fig. 1F). Histological analysis—extent of inflammatory cell infiltrate (ICI), epithelialhyperplasia, goblet cell loss, and distorted crypt structure (Fig. 1G and H)— further established thatBALB/c Lcn2KO mice develop a severe chronic colitis, upon IL-10R neutralization, when compared toWT control.2. Experimental design, materials and methods2.1. MiceLcn2KO mice [6] and their WT littermates on BALB/c background were maintained under specific-pathogen-free conditions in the animal house facility at Pennsylvania State University, PA. Mice werehoused in cages (max. 5 mice per cage) and fed on chow-control diet ad libitum with unrestrictedaccess to water. Animal experiments were approved by the Institutional Animal Care and UseV. Singh et al. / Data in Brief 11 (2017) 588–592590V. Singh et al. / Data in Brief 11 (2017) 588–592 591Committee (IACUC) of Pennsylvania State University. Gut microbiota composition was analyzed inBALB/c Lcn2KO mice and their WT littermates as described in ref. [1].2.2. IL-10R neutralization-induced chronic colitisFour weeks old BALB/c Lcn2KO mice and their WT littermates (n¼4) were administered with fourweekly injections (1.0 mg/mouse, intraperitoneally) of anti-mouse αIL-10R mAb (BioXcell). Controlmice were administered with the isotype (IgG1) control antibody. Colonic inflammation was exam-ined by monitoring for body weight, fecal occult blood, and diarrhea. At one week after the lastinjection of αIL-10R mAb or IgG1 control, the mice were euthanized by CO2 asphyxiation and assessedfor standard chronic colitis parameters.2.3. Enzyme-linked immunosorbent assayBlood samples were collected in a BD Microtainer (Becton Dickinson) via the retro-orbital plexusat euthanasia. Hemolysis-free sera were collected after centrifugation and stored at 80 °C untilfurther analysis. Serum amyloid A (SAA) level was analyzed by ELISA according to the manufacturer's(R & D Systems) protocol.2.4. Quantitative reverse-transcription PCRTotal RNA was isolated from colonic tissue using TRI reagent (Sigma) and used to synthesize cDNAusing the cDNA Synthesis Kit (Quanta BioSciences). qRT-PCR was performed with the use of SYBRGreen Master Mix (Quanta Bio-Sciences) and primers specific for mouse TNF and 36B4 as described inRef. [1], and read using the Step One Plus Real-Time PCR Q28 System (Applied Biosystems).2.5. HistologyAfter euthanasia, mouse colons were prepared as Swiss roll, fixed overnight in 10% neutral buf-fered formalin and stored in 70% ethanol. Colons were processed for paraffin embedding and serialsections (5 mm) were collected and stained with hematoxylin and eosin (H&E) at the Animal Diag-nostic Laboratory, PSU. Histologic scoring was performed as described previously [7].2.6. Statistical analysisData are presented as means7SEM. Statistical significance between the groups was calculatedusing a one-way ANOVA followed by Tukey's multiple comparison test. Po0.05 was consideredstatistically significant. All statistical analyses were performed with the GraphPad Prism 7.0 program(GraphPad, Inc.).Fig. 1. Lcn2 deficiency aggravates colitis upon inhibition of IL-10R signaling. Lcn2-deficient mice (Lcn2KO) and WT littermates(male, n¼4) on BALB/c background were weaned on day 21, and at four weeks of age mice were given interleukin-10 receptor(IL-10R) neutralizing antibody (1.0 mg/mouse, 4 weekly injections; i.p., BioXcell) and monitored for body weights regularly.Control mice received isotype control antibody (rat anti-mouse IgG1). One week post last injection, the mice were euthanizedand analyzed for colitis parameters. (A) Line graph represents percent change in body weight. (B and C) Bar graphs representpercent (B) spleen weight and (C) colon weight. (D) Graph display circulating level of serum amyloid A (SAA), a marker of activeinflammation, measured by ELISA. Colons were harvested, emptied of fecal contents, opened longitudinally and washed in ice-cold PBS. A portion of the proximal colon was collected for qPCR analysis, the remaining colon was used to make Swiss roll forhistological analysis. (E) Relative mRNA level of pro-inflammatory cytokines in the colon. (F) Representative colon images fromcontrol and αIL-10R treated WT and Lcn2KO mice. Right-side panel shows the rectal prolapse (red arrow) in Lcn2KO mice.(G) Image display hematoxylin and eosin (H&E)-stained colonic sections. Red circle shows the inflammatory cell infiltrate (ICI)in the lamina propria and crypt architectural distortion. Black and yellow arrowhead show goblet cell loss and crypt lossrespectively. (H) Histological score was assessed by visualizing the entire H&E-stained colon sections microscopically for theextent of ICI in lamina propria, mucosa and submucosa, epithelial hyperplasia, goblet cell loss, distorted crypt structure,ulcerations and crypt loss. The values are expressed as mean7SEM (*po0.05).V. Singh et al. / Data in Brief 11 (2017) 588–592592AcknowledgementsThis work was supported by grant from the National Institutes of Health R01 (DK097865) to MV-K.VS is supported by CCFA's Research Fellowship Award (ID: 418507).Transparency document. Supplementary materialTransparency data associated with this article can be found in the online version at http://dx.doi.org/10.1016/j.dib.2017.03.002.Appendix A. Supplementary materialSupplementary data associated with this article can be found in the online version at http://dx.doi.org/10.1016/j.dib.2017.03.002.References[1] V. Singh, B.S. Yeoh, B. Chassaing, B. Zhang, P. Saha, X. Xiao, D. Awasthi, R. Shashidharamurthy, M. Dikshit, A. Gewirtz,M. Vijay-Kumar, Microbiota-inducible innate immune, Siderophore Binding Protein Lipocalin 2 is critical for intestinalhomeostasis, Cell. Mol. Gastroenterol. Hepatol. 2 (2016) 482–498 (e6).[2] J.D. Gorham, M.L. Guler, R.G. Steen, A.J. Mackey, M.J. Daly, K. Frederick, W.F. Dietrich, K.M. Murphy, Genetic mapping of amurine locus controlling development of T helper 1/T helper 2 type responses, Proc. Natl. Acad. Sci. USA 93 (1996)12467–12472.[3] J. Yagi, Y. Arimura, H. Takatori, H. Nakajima, I. Iwamoto, T. Uchiyama, Genetic background influences Th cell differentiationby controlling the capacity for IL-2-induced IL-4 production by naive CD4þ T cells, Int. Immunol. 18 (2006) 1681–1690.[4] G.V. Trunova, O.V. Makarova, M.E. Diatroptov, I.M. Bogdanova, L.P. Mikchailova, S.O. Abdulaeva, Morphofunctional char-acteristic of the immune system in BALB/c and C57BL/6 mice, Bull. Exp. Biol. Med. 151 (2011) 99–102.[5] X. Chen, J.J. Oppenheim, O.M. Howard, BALB/c mice have more CD4þCD25þ T regulatory cells and show greater sus-ceptibility to suppression of their CD4þCD25- responder T cells than C57BL/6 mice, J. Leukoc. Biol. 78 (2005) 114–121.[6] T. Berger, A. Togawa, G.S. Duncan, A.J. Elia, A. You-Ten, A. Wakeham, H.E. Fong, C.C. Cheung, T.W. Mak, Lipocalin 2-deficientmice exhibit increased sensitivity to Escherichia coli infection but not to ischemia-reperfusion injury, Proc. Natl. Acad. Sci.USA 103 (2006) 1834–1839.[7] U. Erben, C. Loddenkemper, K. Doerfel, S. Spieckermann, D. Haller, M.M. Heimesaat, M. Zeitz, B. Siegmund, A.A. Kuhl, Aguide to histomorphological evaluation of intestinal inflammation in mouse models, Int. J. Clin. Exp. Pathol. 7 (2014)4557–4576.

Data on IL-10R neutralization-induced chronic colitis in Lipocalin 2 deficient mice on BALB/c background

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Data on IL-10R neutralization-induced chronic colitis in Lipocalin 2 deficient mice on BALB/c background

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