C3h heouj

Manufactured by Jackson ImmunoResearch

Sourced in Montenegro, United States

The C3H/HeOuJ is a laboratory mouse strain. It is a subline of the C3H mouse strain, which is a commonly used inbred strain in biomedical research.

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C3H/HeOuJ male mice C3H/HeOuJ mice Female C3H/HeOuJ mice

17 protocols using c3h heouj

TLR4 Mutant Mice Endotoxin Resistance

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All animal protocols were performed in accordance with the institutional animal care guidelines and conform to the Guide for the Care and Use of Laboratory Animals published by the U.S. National Institutes of Health (NIH Publication, 2011). This study was approved by the Institutional Animal Care and Use Committee (IACUC) of the University Of Louisville School Of Medicine. C3H/HeJ (Tlr4^Lps-d, Stock no.: 000659) and C3H/HeOuJ (Stock no.:000635) mice aged 10–12 weeks were purchased from Jackson Laboratory (Bar Harbor, ME). The C3H/HeJ mice are endotoxin resistant due to a spontaneous mutation at the lipopolysaccharide response locus in the toll-like receptor 4 gene, Tlr4^Lps-d, and we termed these mice as TLR4M hereafter. Whereas the C3H/HeOuJ is a substrain of C3H/HeJ, has normal TLR4, and we termed these mice as TLR4N hereafter. The animals were fed standard chow and regular water ad libitum.

Majumder S., Pushpakumar S., Juin S.K., Jala V.R, & Sen U. (2021). Toll-like receptor 4 mutation protects the kidney from Ang-II-induced hypertensive injury. Pharmacological research, 175, 106030.

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Murine Models for RAGE and TLR4 Studies

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RAGE deficient (ager-/-) mice on a C57/B6 background were generated by Taconic Artemis Pharmaceuticals (Cologne, Germany) for MedImmune and have been described elsewhere [34 (link)]. C3H/HeOuJ (TLR4-sufficient), and C3H/HeJ mice which have defective TLR4 signaling [35 (link)], were purchased from Jackson Laboratories (Bar Harbor, ME). Mice were housed under pathogen-free conditions and were used in experiments at 8–12 weeks of age. All animal experiments were approved by the MedImmune Institutional Animal Use and Care Committee. Human blood from healthy volunteers was obtained with informed consent by venous puncture under MedImmune’s blood donation program. Human monocytic THP-1 and the murine macrophage RAW cell lines were obtained from the American Type Culture Collection (Manassas, VA).

Chen B., Miller A.L., Rebelatto M., Brewah Y., Rowe D.C., Clarke L., Czapiga M., Rosenthal K., Imamichi T., Chen Y., Chang C.S., Chowdhury P.S., Naiman B., Wang Y., Yang D., Humbles A.A., Herbst R, & Sims G.P. (2015). S100A9 Induced Inflammatory Responses Are Mediated by Distinct Damage Associated Molecular Patterns (DAMP) Receptors In Vitro and In Vivo. PLoS ONE, 10(2), e0115828.

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Dietary Modulation of Murine Fibrosis

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All mice were maintained in temperature-controlled, pathogen-free facilities with a 12 h light/dark cycle and given free access to food and water. Male C57BL/6J mice (named B6J), Il4ra−/− mice, and Il4ra+/+ littermate controls were housed at the Universities of Halle and Leipzig. Fibrosis sensitive mouse strain C3H/HeOuJ (hereafter named C3H) were purchased from Jackson Laboratories (2498063-66). Male animals were fed a normal chow diet (9% kcal fat, Ssniff Spezialdiäten; Germany) and euthanized at the age of 18 to 22 weeks. Male C57BL/6J mice were fed an HFD (60% kcal deriving from fat, Research Diets, Inc.) over 6 weeks at the University of Dresden. Mice were injected with recombinant mouse IL-4 (66 μg/kg body weight) complexed with anti-IL-4 (333 μg/kg body weight) or PBS i.p. every other day for the final two weeks of the HFD feeding. Experiments were performed in accordance with the rules of animal care issued by the local government authorities and were approved by the animal care committee of the Universities of Halle, Leipzig, and Dresden, as well as by the state of Saxony and Saxony-Anhalt (Bezirksregierung Leipzig, Bezirksregierung Halle, Germany, T11/21, I11M25, Landesdirektion Sachsen, Germany, TVV57/2018).

Arndt L., Lindhorst A., Neugebauer J., Hoffmann A., Hobusch C., Alexaki V.I., Ghosh A., Blüher M., Wolfrum C., Glaß M, & Gericke M. (2023). The Role of IL-13 and IL-4 in Adipose Tissue Fibrosis. International Journal of Molecular Sciences, 24(6), 5672.

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Murine Model for Controlled Experiments

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Male and Female 5 week-old BALB/cJ, C57BL/6J, C3H/HeJ, or C3H/HeOuJ mice were purchased from Jackson Laboratory (Bar Harbor ME). Mice were acclimatized to the vivarium for a minimum of 10 days after arrival and prior to experimental use. All animals were housed in an ALAAC-approved facility under specific pathogen-free conditions in isolator cages with soft bedding, a 12-hr light/dark schedule, and free access to food and water. All procedures were approved by the Institutional Animal Care at the University of Texas Health Sciences Center San Antonio. During experimental procedures, animals were monitored by laboratory staff daily and general health was evaluated by monitoring body weight, coat appearance, and mobility. Mice were considered morbibund if they lost 30% of their body weight for two consecutive days. Mice maintaining a 30% body weight loss were subsequently euthanized by carbon dioxide exposure. Animal suffering was minimized by providing free access to food and water, animals had soft bedding for the duration of the experiments and all procedures were done under inhaled general anesthesia, 3% isoflurane and oxygen.

Hu Q., Gilley R.P, & Dube P.H. (2019). House dust mite exposure attenuates influenza A infection in a mouse model of pulmonary allergic inflammation. Microbial pathogenesis, 129, 242-249.

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TLR4 Mutant Mice Immune Study

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The National Institutes of Health (NIH) criteria for laboratory animal care were used in this study. Eight week old C3H/HeOuJ (TLR4 WT) and C3H/HeJ (TLR4 mutant) mice were purchased from Jackson Laboratory (Bar Harbor, Maine) and maintained at a NIH animal facility with free access to water and regular chow. This study was approved by the NIDDK, NIH Animal Care and Use Committee.

Souza A.C., Tsuji T., Baranova I.N., Bocharov A.V., Wilkins K.J., Street J.M., Alvarez-Prats A., Hu X., Eggerman T., Yuen P.S, & Star R.A. (2015). TLR4 mutant mice are protected from renal fibrosis and chronic kidney disease progression. Physiological Reports, 3(9), e12558.

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Germ-free C57BL/6J Mice in BSL2 Facility

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SPF C57BL/6 J and C3H/HeOuJ mice were purchased from Jackson Laboratory. Mice were acclimated for at least 72 h prior to experimentation. Germ-free C57BL/6 J mice were provided by the Massachusetts Host-Microbiome Center and following inoculation were maintained with autoclave-sterilized cages, food, and water. Female mice 9-14 weeks of age at the start of experimentation were used. Mice were housed in a temperature (68–75 F) and humidity (50%) controlled facility with 12 h light/dark cycles. Animal studies were conducted in a biosafety level 2 (BSL2) facility at the Brigham and Women’s Hospital. All experiments involving mice were performed according to protocols reviewed and approved by the Brigham and Women’s Hospital Institutional Animal Care and Use Committee (protocol 2016N000416) and in compliance with the Guide for the Care and Use of Laboratory Animals.

Campbell I.W., Hullahalli K., Turner J.R, & Waldor M.K. (2023). Quantitative dose-response analysis untangles host bottlenecks to enteric infection. Nature Communications, 14, 456.

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Transgenic Mice for Intestinal Research

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Six to ten week old male and female wild type (WT) C57Bl/6 mice and TLR2^−/− mice were purchased from Jackson Laboratory (Bar Harbor, ME) as were C3H/HeJ and C3H/HeOuJ (WT controls for C3H/HeJ) mice. Mice that overexpress the anti-apoptotic protein Bcl-2 in the small intestinal epithelium were on an FVB/N background, as previously described (21 (link)). JAM-A^−/− mice (a generous gift of Dr. Charles Parkos) were on a C57Bl/6 background (22 (link)). Similar to WT mice, Bcl-2 transgenic mice, JAM-A^−/− mice, and TLR2^−/− mice were six to ten week old and gender matched. All transgenic and knockout mice were compared to WT mice on the same genetic background (i.e. Bcl-2 transgenic mice were compared to WT FVB/N mice and JAM-A^−/− mice and TLR2^−/− mice were compared to WT C57Bl/6 mice). Mice were kept on a 12 hour light-dark cycle in a dedicated facility managed by the Emory University Division of Animal Resources and received water and mouse chow ad libitum throughout. All experiments were performed in accordance with the National Institutes of Health Guidelines for the Use of Laboratory Animals and were approved by the Institutional Animal Care and Use Committee at Emory University School of Medicine (Protocol DAR-2002717-042217GN).

Meng M., Klingensmith N.J., Liang Z., Lyons J.D., Fay K.T., Chen C.W., Ford M.L, & Coopersmith C.M. (2019). Regulators of intestinal epithelial migration in sepsis. Shock (Augusta, Ga.), 51(1), 88-96.

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C3Ou Mice Infected with C. rodentium

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C3H/HeOuJ (henceforth called C3Ou) (Jackson Laboratory, Bar Harbor, ME) and C3Ou.B6-Cri1 congenic mice [17 (link)] with an introgressed segment of chromosome 15 (entitled Cri-1) from C57BL/6 mice on the C3Ou genomic background were maintained in a specific-pathogen free animal facility at McGill University and provided standard mouse chow and water ad libitum. C. rodentium strain DBS100 was grown overnight in 3 ml of Luria-Bertani (LB) medium shaking at 37°C. Five-week-old mice were infected by oral gavage with 0.1 ml of LB medium containing 2–3 x 10⁸ colony-forming units of bacteria. The infectious dose was confirmed by plating of serial dilutions. Mice were monitored daily and euthanized on experimental days 3, 6, and 9 and their distal colons were dissected and snap frozen in liquid nitrogen for RNA isolation.

Kang E., Yousefi M, & Gruenheid S. (2016). R-Spondins Are Expressed by the Intestinal Stroma and are Differentially Regulated during Citrobacter rodentium- and DSS-Induced Colitis in Mice. PLoS ONE, 11(4), e0152859.

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Hepatocarcinogenesis Model in C3H/HeOuJ Mice

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C3H/HeOuJ male and female mice were purchased from Jackson Laboratory (Bar Harbor, ME), and maintained on a light: dark 12:12 schedule. ZT24/0 is the time of light-on and ZT12 is the time of light-off. Animal studies were approved by the University of North Carolina School of Medicine (Institutional Animal Care and Use Committee).
P15 male C3H/HeOuJ mice were treated with a single intraperitoneal (IP) injection of DEN (Sigma-Aldrich N0258; 20 mg/kg body weight) diluted in 0.85% saline to stimulate hepatocarcinogenesis. Livers from healthy control (−DEN) mice and +DEN mice were collected 25 weeks after treatment at the earliest. Tumors were resected from livers of DEN-treated mice for analysis. Males were used since they reliably develop liver tumors; females do not efficiently biotransform DEN to the ultimate carcinogen and are not suitable for use (44 (link)).

Yang Y., Abdo A.N., Kawara H., Selby C.P, & Sancar A. (2023). Preservation of circadian rhythm in hepatocellular cancer. The Journal of Biological Chemistry, 299(10), 105251.

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Mice Genotypes for TLR and IL-1R Signaling

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All procedures involving mice were performed in accordance with the ARVO Statement for the Use of Animals in Ophthalmology and Vision Research and were approved by the Institutional Animal Care and Use Committee at the University of Miami. To block TLR and IL-1R signaling pathways, we bred rd1 mice with global MyD88 knock-out mice (MyD88^-/-), which have a constitutive deletion of MyD88 exon 3 and show reduced innate immune responses to TLR ligands and IL-1 and IL-18 (Hou et al., 2008 (link)). The rd1 mice (C3H/HeOuJ, The Jackson Laboratory (Bar Harbor, ME, USA), Stock number 000635), are homozygous for the retinal degeneration 1 mutation (Pde6β^rd1) (Bowes et al., 1990 (link); Gibson et al., 2013 (link)) and were bred with MyD88^-/- mice (B6.129P2(SJL)-MyD88^tm1.1Defr/J, Stock number 009088, The Jackson Laboratory) (Hou et al., 2008 (link)) to produce breeders that were homozygous for the rd1 mutation and heterozygous for the MyD88 genotype (MyD88^+/-). The breeders were backcrossed for 4 generations and were used to produce litters containing the rd1/MyD88^+/+ and rd1/MyD88^-/- genotypes. All mice were housed in a 12-hour light/dark cycle and were kept at equivalent distances from the overhead light.

Syeda S., Patel A.K., Lee T, & Hackam A.S. (2015). Reduced photoreceptor death and improved retinal function during retinal degeneration in mice lacking innate immunity adaptor protein MyD88. Experimental neurology, 267, 1-12.

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