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Il 6 mice

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IL-6−/− mice are genetically engineered mice that lack the interleukin-6 (IL-6) gene. These mice are used as a model to study the role of IL-6 in various biological processes and disease conditions.

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Lab products found in correlation

Rag1 mice, by Jackson ImmunoResearch (3 mentions) Thy1 yfp h mice, by Jackson ImmunoResearch (2 mentions) Rosa26 stop dtr mice, by Jackson ImmunoResearch (2 mentions) B6 cd45.1 mice, by Jackson ImmunoResearch (2 mentions) Tnf mice, by Jackson ImmunoResearch (2 mentions) P1530, by Merck Group (2 mentions) C57bl 6j mice, by Beijing Huafukang Biotechnology (2 mentions) C57bl 6j, by Jackson ImmunoResearch (2 mentions) Mle 12, by American Type Culture Collection (1 mentions) Albumin cre mice, by Jackson ImmunoResearch (1 mentions) Wild type c57bl 6j mice, by Jackson ImmunoResearch (1 mentions) Wild type c57bl 6j, by Jackson ImmunoResearch (1 mentions) Cd19 cre mice, by Jackson ImmunoResearch (1 mentions) Pristane, by Merck Group (1 mentions) Tnfr1 2 mice, by Jackson ImmunoResearch (1 mentions) Tnfα mice, by Jackson ImmunoResearch (1 mentions) μmt mice, by Jackson ImmunoResearch (1 mentions) Wild type c57bl 6 mice, by Jackson ImmunoResearch (1 mentions) C57bl 6 mice, by Inotiv (1 mentions)

18 protocols using il 6 mice

1

Transgenic Mouse Models for Dendritic Spine Imaging

Cited 3 times
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Thy1-YFP-H mice (stock 003782)57 (link), which express yellow fluorescent protein (YFP) in L5 pyramidal neurons, Rosa26-stop-DTR mice (stock 007900)58 (link), which express a conditional DTR-encoding allele in the ROSA locus, Rag1−/− mice (stock 002216)59 (link), Tnf−/− mice (stock 005540)60 (link), Il6−/− mice (stock 002650) and B6 CD45.1 mice (stock 002014) were purchased from the Jackson Laboratory. Cx3cr1CreER mice35 (link) were obtained from the laboratory of Wen-Biao Gan (New York University). Cx3cr1GFP mice34 (link) were obtained from the laboratory of Dan Littman (New York University). To image dendritic spine plasticity in Cx3cr1CreER/+;R26iDTR/+ and Tnf−/− mice, these mice were crossed to Thy1-YFP-H mice. For systemic immune challenge, mice were administered poly(I:C) (Sigma P1530; by i.p. injection) that was dissolved in DPBS. Mice were group-housed in temperature-controlled rooms on a 12-h light–dark cycle and were randomly assigned to different treatment groups. The group size was determined based on previous studies using the same methodologies28 (link),29 (link),30 (link),31 (link),32 (link). Both male and female mice were used. All mice were maintained at the NYU Skirball Institute specific-pathogen-free animal facility and handled in accordance with the institutional guidelines for animal care and use.
Garré J.M., Silva H.M., Lafaille J.J, & Yang G. (2017). CX3CR1+ monocytes modulate learning and learning-dependent dendritic spine remodeling via TNFα. Nature medicine, 23(6), 714-722.
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2

Mice Models for Immunological Studies

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C57BL/6, SKG (CREA Japan, Tokyo, Japan), and Il‐6–/– mice (The Jackson Laboratory, Bar Harbor, Maine, USA) were used at 6–10 weeks of age. Animal experiments were reviewed by the Ethics Committee on Animal Experiments of Nippon Medical School (Ethics approval numbers 21–185, 22–115, 22–140, 23–022, 23–184, 23–186, 24–049, 24–143, 27–126, and 2020–082). The study was carried out in accordance with the Guidelines for Animal Experiments of Nippon Medical School, the guidelines of the Law and Notification of the Government of Japan and The ARRIVE Guidelines. Mice were maintained in a 12 h light/12 h dark cycle at 20–24°C with 40%–70% humidity. They were housed at a maximum number of five and were provided with free access to laboratory mouse chow (MF; Oriental Yeast Co, ltd. Tokyo, Japan) and drinking water. All mice were checked for health and stress every day. The animal experiment protocol was approved by the Ethics Committee on Animal Experiments of Nippon Medical School (ethics approval number 26–020, 27–188).
Uehara I., Kajita M., Tanimura A., Hida S., Onda M., Naito Z., Taki S, & Tanaka N. (2022). 2‐Deoxy‐d‐glucose induces deglycosylation of proinflammatory cytokine receptors and strongly reduces immunological responses in mouse models of inflammation. Pharmacology Research & Perspectives, 10(2), e00940.
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3

WT and IL-6 Knockout Mouse Lung Cell Study

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Wild-Type (WT) C57BL/6 and IL-6−/− mice (6-8 weeks old) were purchased from the Jackson Laboratory and bred in-house. An equal proportion of age-matched male and female mice were included in the study. Mice were used in compliance with NIH recommendations for the use of the mice published in the guide for the care and use of lab animals. The animal protocol detailing the procedures and techniques utilized was reviewed and approved by the University of North Dakota Institutional Animal Care and Use Committee (IACUC) under the protocol 1807-9. Mouse lung-epithelial cells (MLE-12) were purchased from ATCC (identifier: ATCCR CRL-2110™) and were cultured and maintained according to the manufacturer’s instructions. A. fumigatus was purchased from American Type Culture Collection (Manassas, VA, USA). A. fumigatus extract was purchased from Greer Laboratories (Lenoir, NC, USA). The Spn serotype 6A strain (BG7322) was obtained from Rochester General Hospital Research Institute (RGHRI) and has been used by us as well as others in the past (10 , 14 (link)).
Schmit T., Ghosh S., Mathur R.K., Barnhardt T., Ambigapathy G., Wu M., Combs C, & Khan M.N. (2020). IL-6 Deficiency Exacerbates Allergic Asthma and Abrogates the Protective Effect of Allergic Inflammation against Streptococcus pneumoniae Pathogenesis. The Journal of Immunology Author Choice, 205(2), 469-479.
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4

Transgenic Mouse Models of Alzheimer's

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The mice used for these studies were hemizygous APPswe/PS1ΔE9 (APP/PS1) and bred on a wild-type C3H/B6 background, C57BL/6j-IL-6tm1Kopf mice (hereafter referred to as IL-6−/− mice), or littermate controls (WT) [23 , 24 (link)].
Original APP/PS1 transgenic breeders as well as IL-6−/− mice were purchased from Jackson Laboratory (Bar Harbor, Maine), and colonies were maintained at Washington University. Equal numbers of male and female mice were used in each study at 2–4 months of age. All studies were performed in accordance with the guidelines of AAALAC and the IACUC at Washington University.
Hettinger J.C., Lee H., Bu G., Holtzman D.M, & Cirrito J.R. (2018). AMPA-ergic regulation of amyloid-β levels in an Alzheimer’s disease mouse model. Molecular Neurodegeneration, 13, 22.
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5

Pneumococcal Pneumosepsis Induction in Mice

Cited 2 times
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C57/BL/6J mice, 7 to 8 weeks old, of both genders were obtained from Beijing Huafukang Bioscience (Beijing, China) and bred at Chongqing Medical University. IL-6−/− mice were purchased from the Jackson Laboratory (Bar Harbor, ME). All animal studies were reviewed and approved by the Animal Ethics Committee of Chongqing Medical University. Mice were anesthetized by 1.5% pentobarbital sodium solution.
Pneumococcal pneumosepsis was induced in anesthetized mice intranasally (i.n.) with 1 × 108 CFU S. pneumoniae D39 suspended in 30 μL phosphate-buffered saline (PBS). This process mimicked the natural route of pneumococcal infection (1 (link), 17 (link), 31 (link)). Bacterial burdens were measured by euthanizing infected mice at the indicated time points and plating serial 10-fold dilutions of each sample onto blood agar plates. Clinical scores were determined as previously described (34 (link)).
Gou X., Xu W., Liu Y., Peng Y., Xu W., Yin Y, & Zhang X. (2022). IL-6 Prevents Lung Macrophage Death and Lung Inflammation Injury by Inhibiting GSDME- and GSDMD-Mediated Pyroptosis during Pneumococcal Pneumosepsis. Microbiology Spectrum, 10(2), e02049-21.
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6

Transgenic Mouse Models for Immunity

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HuLangerin15 , huLangerin-Cre-I-Aβfl16, Batf3−/−17 mice have been previously described. CD90.1 congenic TEa Rag1−/−Cd4 TCR-transgenic to I-Eα52–68 on the C57BL/6 background18 (link) were obtained from M. Jenkins (University of Minnesota), μMT and CD11c-Cre-MHCII from K. Hogquist (University of Minnesota), and IFNAR−/− from M. Mescher (University of Minnesota). IL-6−/− mice on C57BL/6 background were purchased from The Jackson Laboratory. All experiments were performed with 6- to 12-week-old female mice. Mice were housed in microisolator cages and fed irradiated food and acidified water. The University of Minnesota institutional care and use committee approved all mouse protocols.
Yao C., Zurawski S.M., Jarrett E.S., Chicoine B., Crabtree J., Peterson E.J., Zurawski G., Kaplan D.H, & Igyártó B.Z. (2015). Skin DC Induce Follicular Helper T Cells and Protective Humoral Immune Responses. The Journal of allergy and clinical immunology, 136(5), 1387-1397.e7.
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7

Generation of Knockout Mouse Lines

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Albumin-Cre mice and IL-6Rflox/flox mice on a C57BL/6J background were purchased from the Jackson Laboratory (Bar Harbor, ME). IL-6−/− mice and wild-type C57BL/6J mice were purchased from the Jackson Laboratory. IL-22−/− mice on a C57BL/6J background were kindly provided by Dr. Wenjun Ouyang (Genentech, CA) and were further backcrossed to C57BL/6J background in the NIAAA facility for more than 5 generations. Lcn2flox/flox mice were generated as described in Fig. 1. Hepatocyte-specific Lcn2 knockout (Lcn2Hep−/−) and hepatocyte-specific IL-6 receptor knockout (IL-6RHep−/−) mice were generated via several steps that involved crossing Albumin-Cre mice with Lcn2flox/flox and IL-6Rflox/flox mice, respectively. Hepatocyte-specific Stat3 knockout (Stat3Hep−/−) mice were described previously.24 (link)Lcn2 global knockout (Lcn2−/−) mice were obtained from Dr. Tak Mark. Both Lcn2Hep−/− mice and Lcn2−/− mice were backcrossed to a C57BL/6N background for at least 9 generations in the NIAAA animal facility. Littermate Cre-negative floxed mice were used as wild-type (WT) controls for hepatocyte-specific knockout mice. C57BL/6N mice were used as WT controls for Lcn2−/− mice.
Xu M.J., Feng D., Wu H., Wang H., Chan Y., Kolls J., Borregaard N., Porse B., Berger T., Mak T.W., Cowland J.B., Kong X, & Gao B. (2015). The liver is the major source of elevated serum lipocalin-2 levels after bacterial infection or partial hepatectomy: a critical role for IL-6/STAT3. Hepatology (Baltimore, Md.), 61(2), 692-702.
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8

Transgenic Mouse Models for Dendritic Spine Imaging

Cited 3 times
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Thy1-YFP-H mice (stock 003782)57 (link), which express yellow fluorescent protein (YFP) in L5 pyramidal neurons, Rosa26-stop-DTR mice (stock 007900)58 (link), which express a conditional DTR-encoding allele in the ROSA locus, Rag1−/− mice (stock 002216)59 (link), Tnf−/− mice (stock 005540)60 (link), Il6−/− mice (stock 002650) and B6 CD45.1 mice (stock 002014) were purchased from the Jackson Laboratory. Cx3cr1CreER mice35 (link) were obtained from the laboratory of Wen-Biao Gan (New York University). Cx3cr1GFP mice34 (link) were obtained from the laboratory of Dan Littman (New York University). To image dendritic spine plasticity in Cx3cr1CreER/+;R26iDTR/+ and Tnf−/− mice, these mice were crossed to Thy1-YFP-H mice. For systemic immune challenge, mice were administered poly(I:C) (Sigma P1530; by i.p. injection) that was dissolved in DPBS. Mice were group-housed in temperature-controlled rooms on a 12-h light–dark cycle and were randomly assigned to different treatment groups. The group size was determined based on previous studies using the same methodologies28 (link),29 (link),30 (link),31 (link),32 (link). Both male and female mice were used. All mice were maintained at the NYU Skirball Institute specific-pathogen-free animal facility and handled in accordance with the institutional guidelines for animal care and use.
Garré J.M., Silva H.M., Lafaille J.J, & Yang G. (2017). CX3CR1+ monocytes modulate learning and learning-dependent dendritic spine remodeling via TNFα. Nature medicine, 23(6), 714-722.
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9

Aortic Aneurysm in IL-6 Knockout Mice

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C57BL/6J wild‐type (+/+) and IL‐6−/− mice on the same genetic background were obtained from the Jackson Laboratory. Heterozygous mutant mice (Fbn1mgR/+; mgR/+) were obtained from Johns Hopkins University and were bred to generate homozygous mutant mice (Fbn1mgR/mgR; mgR/mgR) and wild‐type littermates (Fbn1+/+; +/+). To create IL‐6−/−•Fbn1mgR/mgR double knockout (DKO) mice, Fbn1mgR/+ were bred with IL‐6‐null mice and offspring bred. For histological analysis of aortic tissues, mice were euthanized at 12 weeks of age. This time point was chosen based on our preliminary studies in which aneurysmal changes were prominent and inflammatory events were evident. All animal experiments were approved by the University of Texas Medical Branch (UTMB) Institutional Animal Care and Use Committee. Mice were housed in the UTMB Animal Resource Center in accordance with the NIH Guidelines for the Care and Use of Animals in Research.
Ju X., Ijaz T., Sun H., LeJeune W., Vargas G., Shilagard T., Recinos A., Milewicz D.M., Brasier A.R, & Tilton R.G. (2014). IL‐6 Regulates Extracellular Matrix Remodeling Associated With Aortic Dilation in a Fibrillin‐1 Hypomorphic mgR/mgR Mouse Model of Severe Marfan Syndrome. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 3(1), e000476.
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10

HOIL-1 KO Mice for Immunological Studies

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HOIL-1 KO mice, with null mutations in the Rbck1 gene that encodes HOIL-1, have been described previously (Tokunaga et al., 2009 (link)). C57BL/6J mice or HOIL-1 WT littermates were used as wild type controls. Rag1−/− mice were purchased from The Jackson Laboratory (Bar Harbor, ME) and bred to HOIL-1 KO mice. Il6−/− mice were purchased from The Jackson Laboratory. Caspase 1;Caspase 11-deficient mice with or without a Caspase 11 transgene were kindly provided by Vishva Dixit, Genentec, San Francisco USA. All mice were housed and bred at Washington University in Saint Louis in specific pathogen-free conditions in accordance with Federal and University guidelines and protocols were approved by the Animal Studies Committee of Washington University under protocol number 20140244. Mice were inoculated between 8 and 11 weeks of age.
MacDuff D.A., Reese T.A., Kimmey J.M., Weiss L.A., Song C., Zhang X., Kambal A., Duan E., Carrero J.A., Boisson B., Laplantine E., Israel A., Picard C., Colonna M., Edelson B.T., Sibley L.D., Stallings C.L., Casanova J.L., Iwai K, & Virgin H.W. (2015). Phenotypic complementation of genetic immunodeficiency by chronic herpesvirus infection. eLife, 4, e04494.
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