Tlr4 mice

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Tlr4−/− mice are genetically modified mice that lack the Toll-like receptor 4 (TLR4) gene. TLR4 is a key component of the innate immune system, playing a crucial role in the recognition of bacterial lipopolysaccharide (LPS) and the subsequent inflammatory response. These mice are a valuable tool for studying the function of TLR4 in various biological processes and disease models.

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TLR4 KO mice (6 citations) TLR4 knockout mice (5 citations) C57BL/10 TLR4 knockout mice (TLR4−/−; C57BL/10ScNJ) (2 citations)

12 protocols using tlr4 mice

Macrophage Differentiation and Paclitaxel Response

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C57BL/6, Nlrp3^−/−, and Tlr4^−/− mice were obtained from The Jackson Laboratory. All mice were maintained under specific pathogen-free conditions and 9~15-weeks-old male mice were used for experiments. In some experiments, mice were intraperitoneally injected with PBS or paclitaxel (40 mg/kg) and sacrificed 24 h post-injection. Mouse bone marrow cells were prepared from the femurs of C57BL/6, Nlrp3^−/−, and Tlr4^−/− mice and cultured in DMEM supplemented with L929 culture supernatants for 5~7 days to differentiate into bone marrow-derived macrophages (BMDMs). Protocols for the animal experiments (2017-0221) were approved by the Institutional Ethical Committee, Yonsei University College of Medicine. All experiments were performed in accordance with the approved guidelines of the Institutional Ethical Committee. BMDMs were maintained in L929-conditioned DMEM supplemented with 10% FBS and antibiotics. A549 cells were grown in DMEM supplemented with 10% FBS and antibiotics.

Son S., Shim D.W., Hwang I., Park J.H, & Yu J.W. (2019). Chemotherapeutic Agent Paclitaxel Mediates Priming of NLRP3 Inflammasome Activation. Frontiers in Immunology, 10, 1108.

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Murine Long-Term Bone Marrow Cultures

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C57BL/6/NHsd and Tlr4^−/− mice were obtained from the Jackson Laboratories (B6.B10ScN-Tlr4^lps-del/JthJ, stock number 007227; Jackson Laboratories, Bar Harbor, ME, USA). LTBMCs were established from the femur and tibia marrow of mice as described elsewhere (4 (link)–8 (link)). The contents of a femur and tibia (N=6/genotype) were flushed into McCoy’s 5A medium (Gibco, Gaithersburg, MD, USA) supplemented with 25% horse serum (Cambrex, Rockland, ME, USA), and 10^–5 M hydrocortisone sodium hemisuccinate. Cultures were incubated at 33°C in 7% CO₂. After four weeks, the horse serum was replaced with 25% fetal bovine serum (FBS) (Thermo Fisher Scientific, Pittsburgh, PA, USA) (6 (link)). Cultures were observed weekly for confluence of the adherent layer of the flasks, hematopoietic cell production, and cobblestone island formation. Cobblestone islands of 50 or more cells were scored weekly in each flask (6 (link), 7 (link)). A two-sided two-sample t-test was used to compare the number of cobblestone islands between Tlr4^−/− and Tlr4^+/+ cultures each week. p-Values less than 0.05 were regarded as significant.

RHIEU B.H., EPPERLY M.W., CAO S., GOFF J., SHIELDS D., FRANICOLA D., WANG H, & GREENBERGER J.S. (2014). Improved Longevity of Hematopoiesis in Long-term Bone Marrow Cultures and Reduced Irradiation-induced Pulmonary Fibrosis in Toll-like Receptor-4 Deletion Recombinant-Negative Mice. In vivo (Athens, Greece), 28(4), 441-448.

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TLR4 Knockout Mice: Immune Response

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C57BL/6 mice were obtained from Charles River Canada (St. Constant, PQ, Canada). TLR4^−/− mice on a C57BL/6 background were obtained from Jackson Laboratories. The mice were housed in Vivarium Service at Victoria Research Laboratories with a 12-hour light/dark cycle and free access to rodent chow and tap water. The experimental protocol followed the institution’s guide for the care and use of laboratory animals and was approved by the Western University Animal Care and Use Committee (Protocol No. 2011–028).

Kao R.L., Xu X., Xenocostas A., Parry N., Mele T., Martin C.M, & Rui T. (2014). Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1. Journal of Inflammation (London, England), 11, 30.

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Immune Response in Genetically Modified Mice

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C57BL6/J (WT), Myd88^−/⁻, Tlr2^−/⁻, and Tlr4^−/⁻ mice (all C57BL6/J strain), purchased from Jackson Laboratory were used in this study. All mice were bred and maintained in a specific pathogen-free (SPF) facility at the UT Southwestern Medical Center. All studies were approved by the Institutional Animal Care and Use Committee (IACUC) and were conducted in accordance with the IACUC guidelines and the National Institutes of Health Guide for the Care and Use of Laboratory Animals. All experimental groups were conducted with age and sex-matched male and female mice. No masking was used during data collection and analysis.

Khan S., Shafiei M.S., Longoria C., Schoggins J.W., Savani R.C, & Zaki H. (2021). SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway. eLife, 10, e68563.

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Genotype-specific Immune Response Study

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C57BL6/J (WT), Myd88^−/−, Tlr2^−/−, and Tlr4^−/− mice (all C57BL6/J strain), purchased from Jackson Laboratory were used in this study. All mice were bred and maintained in a specific pathogen-free (SPF) facility at the UT Southwestern Medical Center. All studies were approved by the Institutional Animal Care and Use Committee (IACUC) and were conducted in accordance with the IACUC guidelines and the National Institutes of Health Guide for the Care and Use of Laboratory Animals. All experimental groups were conducted with age and sex-matched male and female mice.

Khan S., Shafiei M.S., Longoria C., Schoggins J., Savani R.C, & Zaki H. (2021). SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway. bioRxiv.

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Myeloid-specific miR-15a/16 Knockout Mice

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Myeloid specific Cre (004781) and miR-15a/16-null mice (miR-15a/16^-/-) were purchased from Jackson Laboratory (Bar Harbor, Maine) and cross-bred to generate the myeloid specific miR-15a/16^-/- Cre mice. TLR-4^-/- mice were also obtained from Jackson Laboratory. All animals were housed according to the guidelines of the American Association for Laboratory Animal Care and the all protocols were approved by the Animal Research Committee of Brigham and Women's Hospital.

Moon H.G., Yang J., Zheng Y, & Jin Y. (2014). miR-15a/16 Regulates Macrophage Phagocytosis After Bacterial Infection. Journal of immunology (Baltimore, Md. : 1950), 193(9), 4558-4567.

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Evaluation of Immune Responses in Genetically-Modified Mice

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Specific pathogen-free (SPF) age-and sex-matched C57BL/6 mice (wild type, WT) and TLR4^−/− mice were purchased from The Jackson Laboratory (Bar Harbor, ME). IL-36γ^−/− mice on a C57BL/6 background were developed by the Mutant Mouse Regional Resource Center at University of California Davis (Davis, CA). IL-36R^−/− mice on a C57BL/6 background were obtained from Amgen (Thousand Oaks, CA). These mice all displayed normal pulmonary development, were without obvious immune defects in the resting state and reproduced normally. All mice were housed in SPF conditions within the animal care facility (Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, MI) until the day of sacrifice.

Kovach M.A., Singer B., Martinez-Colon G., Newstead M.W., Zeng X., Mancuso P., Moore T.A., Kunkel S.L., Peters-Golden M., Moore B.B, & Standiford T.J. (2017). IL-36γ is a crucial proximal component of protective type-1-mediated lung mucosal immunity in Gram-positive and -negative bacterial pneumonia. Mucosal Immunology, 10(5), 1320-1334.

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Mouse Models for Infection Studies

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C57BL/6, CD45.1 (Ly5.1)-congenic, and Tlr-4^−/− mice were purchased from The Jackson Laboratory. S100a9^−/− and Ager^−/− mice (on a C57BL/6 background) were maintained in our animal colony. Females were used for all experiments except C. difficile infections, and all mice were between 9 and 14 weeks of age at the time of infection. Specifically, mice fed custom-synthesized diets were 12–14 weeks old at the time of infection. Mice in Figure 4A and Supplementary Figure 3B were 8–9 weeks old at the time of infection and fed normal chow prior to infection. C. difficile infection studies were conducted on adult (8 to 12 week old) age-matched male C57BL/6 mice. Typical weight and food intake data is included in Supplementary Figure 1A & B. Mice were housed, 5 to a cage, in specific pathogen free conditions. Food and water was provided ad libitum. Mice were assigned to experimental groups using a random number generator. All animal experiments were approved and performed in compliance with the Vanderbilt Institutional Animal Care and Use Committee (IACUC).

Juttukonda L.J., Berends E.T., Zackular J.P., Moore J.L., Stier M.T., Zhang Y., Schmitz J.E., Beavers W.N., Wijers C.D., Gilston B.A., Kehl-Fie T.E., Atkinson J., Washington M.K., Peebles R.S., Chazin W.J., Torres V.J., Caprioli R.M, & Skaar E.P. (2017). Dietary manganese promotes staphylococcal infection of the heart. Cell host & microbe, 22(4), 531-542.e8.

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Casp-11 and Tlr4 Knockout Mice

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C57BL/6 WT, Casp-11^−/− and Tlr4^−/− mice were purchased from Jackson Laboratory. All mice used in this study were bred and maintained in a specific pathogen-free facility at New York University Medical Center. All experiments were performed according to the experimental protocols approved by the Institutional Animal Care and Use Committee of New York University.

Yi Y.S., Jian J., Gonzalez-Gugel E., Shi Y.X., Tian Q., Fu W., Hettinghouse A., Song W., Liu R., He M., Qi H., Yang J., Du X., Xiao G., Chen L, & Liu C.J. (2018). p204 Is Required for Canonical Lipopolysaccharide-induced TLR4 Signaling in Mice. EBioMedicine, 29, 78-91.

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Isolation of Pulmonary Fibroblasts from WT and TLR4-/- Mice

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Wild type (WT) C57BL/6 mice and TLR4^-/- mice (Jackson Labs, on a C57BL/6 genetic background) were used in this study. All experiments involving live animals were carried out in accordance with the National Institutes of Health guidelines for the use of experimental animals (41 ) and were reviewed and approved by the Institutional Animal Care and Use Committee (IACUC) at the Feinstein Institutes for Medical Research. The lungs of 4-8-week-old WT and TLR4^-/- mice were explanted, and each group of pulmonary fibroblasts was isolated from a pool of 3-4 lungs, as previously described (42 (link)). The isolated fibroblasts were then cultured in DMEM supplemented with 10% heat-inactivated fetal bovine serum (FBS, MP Biomedicals), 2% penicillin-streptomycin, and L-glutamine (Gibco, ThermoFisher Scientific).

Bolourani S., Sari E., Brenner M, & Wang P. (2021). Extracellular CIRP Induces an Inflammatory Phenotype in Pulmonary Fibroblasts via TLR4. Frontiers in Immunology, 12, 721970.

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