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Journal articles on the topic 'C57BL/6 wild-type mice'

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Published: 5 June 2025

Last updated: 1 August 2025

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1

Durmus, Nedim, Wen-Chi Chen, Sung-Hyun Park та ін. "Resistin-like Molecule α and Pulmonary Vascular Remodeling: A Multi-Strain Murine Model of Antigen and Urban Ambient Particulate Matter Co-Exposure". International Journal of Molecular Sciences 24, № 15 (2023): 11918. http://dx.doi.org/10.3390/ijms241511918.

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Pulmonary hypertension (PH) has a high mortality and few treatment options. Adaptive immune mediators of PH in mice challenged with antigen/particulate matter (antigen/PM) has been the focus of our prior work. We identified key roles of type-2- and type-17 responses in C57BL/6 mice. Here, we focused on type-2-response-related cytokines, specifically resistin-like molecule (RELM)α, a critical mediator of hypoxia-induced PH. Because of strain differences in the immune responses to type 2 stimuli, we compared C57BL/6J and BALB/c mice. A model of intraperitoneal antigen sensitization with subseque

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2

Kenyon, Nicholas J., Albert van der Vliet, Bettina C. Schock, Tatsuya Okamoto, Gabrielle M. McGrew, and Jerold A. Last. "Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 3 (2002): L540—L545. http://dx.doi.org/10.1152/ajplung.00297.2001.

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Mice deficient in inducible nitric oxide synthase (iNOS; C57Bl/6Ai-[KO] NOS2 N5) or wild-type C57Bl/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclea

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3

SINGH, Uma, Shumei ZHONG, Momiao XIONG, Tong-bin LI, Allan SNIDERMAN, and Ba-Bie TENG. "Increased plasma non-esterified fatty acids and platelet-activating factor acetylhydrolase are associated with susceptibility to atherosclerosis in mice." Clinical Science 106, no. 4 (2004): 421–32. http://dx.doi.org/10.1042/cs20030375.

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Animal models provide vital tools to explicate the pathogenesis of atherosclerosis. Accordingly, we established two atherosclerosis-prone mice models: (i) mice lacking the LDL (low-density lipoprotein) receptor (LDLR) and the ability to edit apo (apolipoprotein) B mRNA (Apobec1; designated LDb: LDLR-/-Apobec1-/-), and (ii) mice with the LDb background, who also overexpressed human apoB100 (designated LTp: LDLR-/-Apobec1-/-ERhB+/+). Both LDb and LTp mice had markedly elevated levels of LDL and increased levels of NEFAs (non-esterified fatty acids) compared with C57BL/6 wild-type mice. However,

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4

Pappo, Jacques, Deirdre Torrey, Lillian Castriotta, Anneli Savinainen, Zita Kabok, and Alexander Ibraghimov. "Helicobacter pylori Infection in Immunized Mice Lacking Major Histocompatibility Complex Class I and Class II Functions." Infection and Immunity 67, no. 1 (1999): 337–41. http://dx.doi.org/10.1128/iai.67.1.337-341.1999.

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ABSTRACT The role of major histocompatibility complex (MHC) class I- and class II-restricted functions in Helicobacter pyloriinfection and immunity upon oral immunization was examined in vivo. Experimental challenge with H. pylori SS1 resulted in significantly greater (P ≤ 0.025) colonization of MHC class I and class II mutant mice than C57BL/6 wild-type mice. Oral immunization with H. pylori whole-cell lysates and cholera toxin adjuvant significantly reduced the magnitude of H. pylori infection in C57BL/6 wild-type (P = 0.0083) and MHC class I knockout mice (P = 0.0048), but it had no effect

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5

Akoum, J., K. Tahiri, F. Etienne, M. T. Corvol, F. Rannou, and C. Nguyen. "AB0063 AGING CARTILAGE IN WILD-TYPE MICE: AN OBSERVATIONAL STUDY." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1333.2–1333. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5989.

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Background:Many animal models of osteoarthritis (OA) have been used to study the pathogenesis of cartilage degeneration1. In mice, spontaneous OA can occur in wild-type or genetically modified animals. The first report of spontaneous OA developing in wild-type mice was published in 19562and changes affecting the knee joint were further related to OA by using ultrastructural- histochemical analyses. However, a quantitative assessment of age-related evolution of OA-type cartilage lesions is lacking. The OA Research Society International (OARSI) grading score was adapted to semi-quantify histopat

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6

Zhong, Zifu, João Paulo Portela Catani, Séan Mc Cafferty, et al. "Immunogenicity and Protection Efficacy of a Naked Self-Replicating mRNA-Based Zika Virus Vaccine." Vaccines 7, no. 3 (2019): 96. http://dx.doi.org/10.3390/vaccines7030096.

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To combat emerging infectious diseases like Zika virus (ZIKV), synthetic messenger RNAs (mRNAs) encoding viral antigens are very attractive as they allow a rapid, generic, and flexible production of vaccines. In this work, we engineered a self-replicating mRNA (sr-mRNA) vaccine encoding the pre-membrane and envelope (prM-E) glycoproteins of ZIKV. Intradermal electroporation of as few as 1 µg of this mRNA-based ZIKV vaccine induced potent humoral and cellular immune responses in BALB/c and especially IFNAR1-/- C57BL/6 mice, resulting in a complete protection of the latter mice against ZIKV infe

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7

Curran, Shelly, and Joseph Kovacs. "Altered Trained immunity in AID−/− versus wild type mice following infection with Pneumocystis murina." Journal of Immunology 208, no. 1_Supplement (2022): 58.12. http://dx.doi.org/10.4049/jimmunol.208.supp.58.12.

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Abstract Pneumocystis pneumonia continues to be a life-threatening infection in immunocompromised individuals. Dendritic cells are key antigen presenters to CD4+ T cells, which are critical to controlling Pneumocystis infection along with B cells. β-1,3 glucans are found in the cell wall of the cyst form of Pneumocystis. Glucans derived from other fungi have been shown to induce trained immunity. Therefore, we explored if Pneumocystis infection can induce a trained immunity response in C57Bl/6 (wild type) mice following exposure via a natural route of infection. We also tested activation-induc

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8

Kopić, Alexandra, Karima Benamara, Maria Schuster, et al. "Coagulation phenotype of wild-type mice on different genetic backgrounds." Laboratory Animals 53, no. 1 (2018): 43–52. http://dx.doi.org/10.1177/0023677218811059.

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Genetically engineered mouse models are used to investigate beneficial treatment in haemophilia by comparison with wild-type mice. It has been recognized that wild-type and haemophilic mice of different genetic backgrounds show different bleeding phenotypes. We assessed ex-vivo coagulation parameters in nine wild-type substrains of 129S1/Sv, BALB/c and C57BL/6 mice applying thromboelastography (TEG), activated partial thromboplastin time (aPTT), prothrombin time (PT) and fibrinogen levels. The comprehensive ex-vivo data are discussed in view of results from a tail-tip bleeding assay. Time to f

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9

Hertz, Cheryl J., Hanna Filutowicz та John M. Mansfield. "Resistance to the African Trypanosomes Is IFN-γ Dependent". Journal of Immunology 161, № 12 (1998): 6775–83. http://dx.doi.org/10.4049/jimmunol.161.12.6775.

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Abstract The role of variant surface glycoprotein (VSG)-specific Th cell responses in determining resistance to the African trypanosomes was examined by comparing Th cell responses in relatively resistant and susceptible mice as well as in cytokine gene knockout mice infected with Trypanosoma brucei rhodesiense. Resistant B10.BR and C57BL/6 mice expressed Th1 cell cytokine responses to VSG stimulation during infection, while susceptible C3H mice produced weak or no Th1 cell cytokine responses. Neither resistant B10.BR and C57BL/6 mice nor susceptible C3H mice made detectable Th2 cell cytokine

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Boesteanu, Alina C., Jillian A. Norton, Martin Turner, and Peter D. Katsikis. "The role of p110delta in the immunopathology of influenza virus infection (130.12)." Journal of Immunology 182, no. 1_Supplement (2009): 130.12. http://dx.doi.org/10.4049/jimmunol.182.supp.130.12.

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Abstract Infection of C57Bl/6 mice with influenza virus is accompanied by morbidity manifested as weight loss and lung pathology. We have found that mice that have an inactivating mutation in the leucocyte-specific phosphoinositide kinase 3 (PIK3) isoform p110delta (p110delta-/- on a C57BL/6 background manifest significantly reduced morbidity after influenza virus infection compared to C57BL/6 mice. RAG-/- mice also showed reduced morbidity compared to wild type animals, indicating a role for lymphocytes in this pathology. At day 6 postinfection activated pulmonary T cells and NK cells were gr

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11

Brunet, L. R., F. D. Finkelman, A. W. Cheever, M. A. Kopf, and E. J. Pearce. "IL-4 protects against TNF-alpha-mediated cachexia and death during acute schistosomiasis." Journal of Immunology 159, no. 2 (1997): 777–85. http://dx.doi.org/10.4049/jimmunol.159.2.777.

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Abstract To examine the role of the Th2-type response during schistosomiasis mansoni we compared disease progression in wild type (wt), and Th2-response deficient IL-4(-/-) mice. Whereas wt C57BL/6 mice tolerate infection and develop chronic disease, IL-4(-/-) C57BL/6 animals are highly susceptible, exhibiting severe acute cachexia followed by death. Data point toward morbidity in the IL-4(-/-) C57BL/6 mice being mediated by TNF-alpha, possibly through the uncontrolled production of nitric oxide in target organs such as the ileum. We propose that IL-4 prevents severe disease during schistosomi

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12

Morris, Suzanne C., Stephanie Ruwe, Jane Scott, and Fred D. Finkelman. "IL-4 regulates CD8+ T cell homeostasis in BALB/c but not C57BL/6 mice (97.8)." Journal of Immunology 182, no. 1_Supplement (2009): 97.8. http://dx.doi.org/10.4049/jimmunol.182.supp.97.8.

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Abstract Because IL-4 potently stimulates murine CD8+ T cell proliferation during an in vivo Th2 response, we evaluated whether IL-4 also contributes to CD8+ T cell homeostasis in naïve mice. Adult, wild-type BALB/c mice have ~2x the number of total and ~5x the number of memory phenotype (CD44highLy6Chigh) splenic CD8+ T cells as IL-4-, IL-4Rα- and Stat6-deficient BALB/c mice. Rare, IL-4-dependent, memory phenotype CD8+ T cells are found in BALB/c thymus by week 2 of life. The effects of IL-4-deficiency on CD8+ T cells can be reproduced by treating pregnant mice and then their offspring with

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13

Akimoto, Toshihiko, Fumio Numata, Misato Tamura, et al. "Abrogation of Bronchial Eosinophilic Inflammation and Airway Hyperreactivity in Signal Transducers and Activators of Transcription (STAT)6-deficient Mice." Journal of Experimental Medicine 187, no. 9 (1998): 1537–42. http://dx.doi.org/10.1084/jem.187.9.1537.

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Signal transducers and activators of transcription 6 (STAT6) is essential for interleukin 4–mediated responses, including class switching to IgE and induction of type 2 T helper cells. To investigate the role of STAT6 in allergic asthma in vivo, we developed a murine model of allergen-induced airway inflammation. Repeated exposure of actively immunized C57BL/6 mice to ovalbumin (OVA) aerosol increased the level of serum IgE, the number of eosinophils in bronchoalveolar lavage (BAL) fluid, and airway reactivity. Histological analysis revealed peribronchial inflammation with pulmonary eosinophil

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14

Nagayama, Masao, Tracy Aber, Tomiko Nagayama, M. Elizabeth Ross, and Constantino Iadecola. "Age-Dependent Increase in Ischemic Brain Injury in Wild-Type Mice and in Mice Lacking the Inducible Nitric Oxide Synthase Gene." Journal of Cerebral Blood Flow & Metabolism 19, no. 6 (1999): 661–66. http://dx.doi.org/10.1097/00004647-199906000-00009.

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The authors investigated the influence of age on the outcome of cerebral ischemia in wild-type mice and in mice with a deletion of the inducible nitric oxide synthase (iNOS) gene. The middle cerebral artery was permanently occluded in iNOS-null mice and in wild-type (C57BL/6) controls aged 4, 8, 16, and 24 weeks. Infarct volume was determined in thionin-stained brain sections 4 days after permanent middle cerebral artery occlusion. No differences in forebrain volume were found among wild-type and iNOS-null mice at the ages studied (P> 0.05). In C57BL/6 mice (n = 5 to 6/group), neocortical i

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15

Vierboom, Michel P. M., Hans W. Nijman, Rienk Offringa, et al. "Tumor Eradication by Wild-type p53-specific Cytotoxic T Lymphocytes." Journal of Experimental Medicine 186, no. 5 (1997): 695–704. http://dx.doi.org/10.1084/jem.186.5.695.

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The tumor suppressor protein p53 is overexpressed in close to 50% of all human malignancies. The p53 protein is therefore an attractive target for immunotherapy. Cytotoxic T lymphocytes (CTLs) recognizing a murine wild-type p53 peptide, presented by the major histocompatibility complex class I molecule H-2Kb, were generated by immunizing p53 gene deficient (p53 −/−) C57BL/6 mice with syngeneic p53-overexpressing tumor cells. Adoptive transfer of these CTLs into tumor-bearing p53 +/+ nude mice caused complete and permanent tumor eradication. Importantly, this occurred in the absence of any demo

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16

Pan, Pan, Chad W. Skaer, Hsin-Tzu Wang, et al. "Systemic Metabolite Changes in Wild-type C57BL/6 Mice Fed Black Raspberries." Nutrition and Cancer 69, no. 2 (2017): 299–306. http://dx.doi.org/10.1080/01635581.2017.1263748.

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17

Mott, Kevin R., Guey-Chuen Perng, Yanira Osorio, Konstantin G. Kousoulas, and Homayon Ghiasi. "A Recombinant Herpes Simplex Virus Type 1 Expressing Two Additional Copies of gK Is More Pathogenic than Wild-Type Virus in Two Different Strains of Mice." Journal of Virology 81, no. 23 (2007): 12962–72. http://dx.doi.org/10.1128/jvi.01442-07.

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ABSTRACT The effect of glycoprotein K (gK) overexpression on herpes simplex virus type 1 (HSV-1) infection in two different strains of mice was evaluated using a recombinant HSV-1 virus that expresses two additional copies of the gK gene in place of the latency-associated transcript (LAT). This mutant virus (HSV-gK3) expressed higher levels of gK than either the wild-type McKrae virus or the parental dLAT2903 virus both in vitro (in cultured cells) and in vivo (in infected mouse corneas and trigeminal ganglia [TG] of BALB/c and C57BL/6 mice). gK transcripts were detected in the TG of both HSV-

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18

Couldrey, Christine, Heath L. Bradley, and Kevin D. Bunting. "A STAT5 modifier locus on murine chromosome 7 modulates engraftment of hematopoietic stem cells during steady-state hematopoiesis." Blood 105, no. 4 (2005): 1476–83. http://dx.doi.org/10.1182/blood-2004-06-2302.

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AbstractHomologous disruption of expression of signal transducer and activator of transcription 5a (STAT5a) and STAT5b (STAT5ab–/–) in mice results in hematopoietic stem cells (HSCs) that can engraft irradiated hosts alone but are noncompetitive against wild-type HSCs. To explore mechanisms for this phenotype, we crossed the STAT5 mutations onto an HW80 background congenic to the original C57BL/6 that differs in a small chromosome 7 genomic locus. We previously demonstrated that C57BL/6 or HW80 background STAT5ab–/– bone marrow (BM) cells showed equal repopulating function either competitively

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Kang, Tae Jin, Annamneedi Venkata Venkata Prakash, and Juwon Seong. "The Role of Circadian Clock Period 2 (per 2) gene and the expression of per2 related gene in atopic dermatitis animal model." Journal of Immunology 204, no. 1_Supplement (2020): 147.13. http://dx.doi.org/10.4049/jimmunol.204.supp.147.13.

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Abstract Atopic dermatitis is a chronic, inflammatory skin disorder associated with defective skin barrier and epidermal hyper reactivity. AD is a Th2 mediated allergic disease. GATA3 is a transcription factor that plays an important role in Th2 differentiation. In this study we investigated the per2 gene role and the expression of per2 related genes in atopic dermatitis. We established the atopic dermatitis animal model in per2 knock out and C57BL/6 by 2,4-dinitrochlorobenzene (DNCB). A subset of mice in both per2 knock out and C57BL/6 were treated with saline as control group. The skin lesio

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TOENJES, S. A., R. J. SPOLSKI, K. A. MOONEY та R. E. KUHN. "γδT cells do not play a major role in controlling infection in experimental cysticercosis". Parasitology 119, № 4 (1999): 413–18. http://dx.doi.org/10.1017/s0031182099004771.

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Protective immunity against larval Taenia crassiceps has been shown to rely on T cells; however, the roles of the specific subsets of T cells during infection are not known. To investigate a possible role for γδT cells, this study investigated larval infection in δ-chain knock-out C57BL/6 (deltaKO) and wild-type C57BL/6 mice. It was found that deltaKO mice and C57BL/6 mice were equally susceptible to infection suggesting γδT cells do not play a major role in protective immunity. Cytokine production by concanavalin A (ConA)-stimulated spleen cells from infected deltaKO mice and C57BL/6 mice wer

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Zhang, Guang-Xian, Bao-Guo Xiao, Xue-Feng Bai, Peter H. van der Meide, Anders Örn та Hans Link. "Mice with IFN-γ Receptor Deficiency Are Less Susceptible to Experimental Autoimmune Myasthenia Gravis". Journal of Immunology 162, № 7 (1999): 3775–81. http://dx.doi.org/10.4049/jimmunol.162.7.3775.

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Abstract IFN-γ can either adversely or beneficially affect certain experimental autoimmune diseases. To study the role of IFN-γ in the autoantibody-mediated experimental autoimmune myasthenia gravis (EAMG), an animal model of myasthenia gravis in humans, IFN-γR-deficient (IFN-γR−/−) mutant C57BL/6 mice and congenic wild-type mice were immunized with Torpedo acetylcholine receptor (AChR) plus CFA. IFN-γR−/− mice exhibited significantly lower incidence and severity of muscle weakness, lower anti-AChR IgG Ab levels, and lower Ab affinity to AChR compared with wild-type mice. Passive transfer of s

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Cusick, Matthew, Jane Libbey, and Robert Fujinami. "A few changes in wild-type picornavirus genome lead to immunosuppression (VIR8P.1068)." Journal of Immunology 192, no. 1_Supplement (2014): 209.4. http://dx.doi.org/10.4049/jimmunol.192.supp.209.4.

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Abstract Viruses, such as human immunodeficiency virus and poliovirus, use a variety of mechanisms to suppress the immune response and evade clearance by the host. Therefore, investigating how a few changes in the viral genome of a non-lethal virus can lead to an alteration in disease, from survivable to immunosuppression and death, would provide valuable information into viral pathogenesis. Here we investigate a picornavirus, the Theiler’s murine encephalomyelitis virus (TMEV), in its natural host, the mouse. C57BL/6 mice infected intracerebrally (i.c.) with the DA strain of TMEV develop acut

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Murthy, Ashlesh K., Weidang Li, Bharat K. R. Chaganty, et al. "Tumor Necrosis Factor Alpha Production from CD8+T Cells Mediates Oviduct Pathological Sequelae following Primary Genital Chlamydia muridarum Infection." Infection and Immunity 79, no. 7 (2011): 2928–35. http://dx.doi.org/10.1128/iai.05022-11.

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ABSTRACTThe immunopathogenesis ofChlamydia trachomatis-induced oviduct pathological sequelae is not well understood. Mice genetically deficient in perforin (perforin−/−mice) or tumor necrosis factor alpha (TNF-α) production (TNF-α−/−mice) displayed comparable vaginal chlamydial clearance rates but significantly reduced oviduct pathology (hydrosalpinx) compared to that of wild-type mice. Since both perforin and TNF-α are effector mechanisms of CD8+T cells, we evaluated the role of CD8+T cells during genitalChlamydia muridaruminfection and oviduct sequelae. Following vaginal chlamydial challenge

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Magez, Stefan, Magdalena Radwanska, Alain Beschin, Kenji Sekikawa, and Patrick De Baetselier. "Tumor Necrosis Factor Alpha Is a Key Mediator in the Regulation of Experimental Trypanosoma brucei Infections." Infection and Immunity 67, no. 6 (1999): 3128–32. http://dx.doi.org/10.1128/iai.67.6.3128-3132.1999.

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ABSTRACT In order to evaluate during experimental Trypanosoma brucei infections the potential role of tumor necrosis factor alpha (TNF-α) in the host-parasite interrelationship, C57BL/6 TNF-α knockout mice (TNF-α−/−) as well as C57BL/6 wild-type mice were infected with pleomorphic T. bruceiAnTat 1.1 E parasites. In the TNF-α−/− mice, the peak levels of parasitemia were strongly increased compared to the peak levels recorded in wild-type mice. The increased parasite burden did not reflect differences in clearance efficacy or in production ofT. brucei-specific immunoglobulin M (IgM) and IgG anti

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Fol, Marek, Marcin Włodarczyk, Magdalena Kowalewicz-Kulbat, et al. "Mycobacterium bovis Wild-Type BCG or Recombinant BCG Secreting Murine IL-18 (rBCG/IL-18) Strains in Driving Immune Responses in Immunocompetent or Immunosuppressed Mice." Vaccines 10, no. 4 (2022): 615. http://dx.doi.org/10.3390/vaccines10040615.

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Mycobacterium tuberculosis infections remain a global health problem in immunosuppressed patients. The effectiveness of BCG (Bacillus Calmette–Guérin), an anti-tuberculosis vaccine, is unsatisfactory. Finding a new vaccine candidate is a priority. We compared numerous immune markers in BCG-susceptible C57BL/6 and BCG-resistant C3H mice who had been injected with 0.9% NaCl (control) or with wild-type BCG or recombinant BCG secreting interleukin (IL)-18 (rBCG/IL-18) and in immunized mice who were immunocompromised with cyclophosphamide (CTX). The inoculation of rBCG/IL-18 in immunocompetent mice

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Walker, David H., Juan P. Olano, and Hui-Min Feng. "Critical Role of Cytotoxic T Lymphocytes in Immune Clearance of Rickettsial Infection." Infection and Immunity 69, no. 3 (2001): 1841–46. http://dx.doi.org/10.1128/iai.69.3.1841-1846.2001.

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ABSTRACT Cytotoxic T-lymphocyte (CTL) activity developed against the major infected target cells of rickettsial infections, endothelial cells and macrophages. Spleen cells from mice immune to Rickettsia conorii exerted specific major histocompatibility complex (MHC) class I-matched CTL activity against R. conorii-infected SVEC-10 endothelial cells, with peak activity on day 10. Similarly, spleen cells from Rickettsia australis-immune mice exerted specific CTL activity against an R. australis-infected macrophage-like cell line. Gamma interferon (IFN-γ) gene knockout mice were more than 100-fold

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Wei, Qingqing, Xiao-Ming Yin, Mong-Heng Wang, and Zheng Dong. "Bid deficiency ameliorates ischemic renal failure and delays animal death in C57BL/6 mice." American Journal of Physiology-Renal Physiology 290, no. 1 (2006): F35—F42. http://dx.doi.org/10.1152/ajprenal.00184.2005.

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Tubular cell apoptosis is involved in ischemic renal failure, but the underlying mechanism is unclear. Bid, a proapoptotic Bcl-2 family protein, may regulate the intrinsic as well as the extrinsic pathway of apoptosis. In vivo, Bid is most abundantly expressed in the kidneys. However, the role played by Bid in renal pathophysiology is unknown. Our recent work demonstrated Bid activation during renal ischemia-reperfusion. The current study has determined the role of Bid in ischemic renal injury and renal failure using Bid-deficient mice. In wild-type C57BL/6 mice, Bid was proteolytically proces

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Mansfield, L. S., J. A. Bell, D. L. Wilson, et al. "C57BL/6 and Congenic Interleukin-10-Deficient Mice Can Serve as Models of Campylobacter jejuni Colonization and Enteritis." Infection and Immunity 75, no. 3 (2006): 1099–115. http://dx.doi.org/10.1128/iai.00833-06.

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ABSTRACT Campylobacter jejuni is a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized that C. jejuni 11168 colonizes the gastrointestinal tract of both C57BL/6 mice and congenic C57BL/6 interleukin-10-deficient (IL-10−/−) mice and that C57BL/6 IL-10−/− mice experience C. jejuni 11168-mediated clinical signs and pathology. Individually housed mice were challenged orally with C. jejuni 11168, and the course of infection was monitored by clinical examination, bacterial culture, C. jejuni-specific PCR, gross path

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Denison, Amy M., Brenda Clapper, and Kevin Dybvig. "Avoidance of the Host Immune System through Phase Variation in Mycoplasma pulmonis." Infection and Immunity 73, no. 4 (2005): 2033–39. http://dx.doi.org/10.1128/iai.73.4.2033-2039.2005.

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ABSTRACT Phase-variable lipoproteins are commonly found in Mycoplasma species. Mycoplasma pulmonis contains a family of extensively studied phase- and size-variable lipoproteins encoded by the vsa locus. The Vsa surface proteins vary at a high frequency, the in vivo significance of which has yet to be determined. We investigated the role of Vsa phase variation in respect to tissue tropism and avoidance of the immune system in the mouse host. Mycoplasmas were cultured 3, 14, and 21 days postinoculation from the nose, lung, trachea, liver, and spleen of experimentally infected C57BL/6 (wild-type

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Egecioglu, Emil, Karolina Ploj, Xiufeng Xu, et al. "Central NMU signaling in body weight and energy balance regulation: evidence from NMUR2 deletion and chronic central NMU treatment in mice." American Journal of Physiology-Endocrinology and Metabolism 297, no. 3 (2009): E708—E716. http://dx.doi.org/10.1152/ajpendo.91022.2008.

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To investigate the role of the central neuromedin U (NMU) signaling system in body weight and energy balance regulation, we examined the effects of long-term intracerebroventricular (icv) infusion of NMU in C57Bl/6 mice and in mice lacking the gene encoding NMU receptor 2. In diet-induced obese male and female C57BL/6 mice, icv infusion of NMU (8 μg·day−1·mouse−1) for 7 days decreased body weight and total energy intake compared with vehicle treatment. However, these parameters were unaffected by NMU treatment in lean male and female C57BL/6 mice fed a standard diet. In addition, female (but n

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Pena Rossi, Claudia, Andrés McAllister, Myriam Tanguy, David Kägi, and Michel Brahic. "Theiler’s Virus Infection of Perforin-Deficient Mice." Journal of Virology 72, no. 5 (1998): 4515–19. http://dx.doi.org/10.1128/jvi.72.5.4515-4519.1998.

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ABSTRACT Theiler’s virus, a murine picornavirus, infects the central nervous systems of C57BL/6 mice and is cleared after approximately 10 days by a process which requires CD8+ cytotoxic T cells. We used perforin-deficient C57BL/6 mice to test the role of this protein in viral clearance. Perforin-deficient mice died from viral encephalomyelitis between days 12 and 18 postinoculation. They had high levels of viral RNA in their central nervous systems until the time of death. In contrast, viral RNA had disappeared by day 11 postinoculation in wild-type C57BL/6 mice. Cytotoxic T cells can kill in

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Liu, Cuihua, Kaoru Tanaka, Takanori Katsube, et al. "Altered Response to Total Body Irradiation of C57BL/6-Tg (CAG-EGFP) Mice." Dose-Response 18, no. 3 (2020): 155932582095133. http://dx.doi.org/10.1177/1559325820951332.

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Application of green fluorescent protein (GFP) in a variety of biosystems as a unique bioindicator or biomarker has revolutionized biological research and made groundbreaking achievements, while increasing evidence has shown alterations in biological properties and physiological functions of the cells and animals overexpressing transgenic GFP. In this work, response to total body irradiation (TBI) was comparatively studied in GFP transgenic C57BL/6-Tg (CAG-EGFP) mice and C57BL/6 N wild type mice. It was demonstrated that GFP transgenic mice were more sensitive to radiation-induced bone marrow

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Yang, Xing-Tang, and Zhi-Jun Wang. "CD177 Expression and Inflammation Grade in Helicobacter pylori-Infected Wild-Type and CD177-/- C57BL/6 Mice." Analytical Cellular Pathology 2019 (April 4, 2019): 1–6. http://dx.doi.org/10.1155/2019/9506863.

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This study was undertaken to further investigate the CD177 expression in Helicobacter pylori- (Hp-) infected wild-type and CD177-/- C57BL/6 mice, which may be helpful to elucidate the relationship between CD177 and Hp-related gastritis. 20 WT mice were randomly assigned into the Hpss1 WT group (n=10) and Hp49503 WT group (n=10); 20 KO mice were randomly assigned into the Hpss1 KO group (n=10) and Hp49503 KO group (n=10). The remaining mice served as controls. Mice in the HpSS1 groups and Hp49503 groups were independently infected with corresponding strains. Results showed that the Hp colonizat

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Nishie, Hideaki, Akiko Nakano-Doi, Toshinori Sawano, and Takayuki Nakagomi. "Establishment of a Reproducible Ischemic Stroke Model in Nestin-GFP Mice with High Survival Rates." International Journal of Molecular Sciences 22, no. 23 (2021): 12997. http://dx.doi.org/10.3390/ijms222312997.

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An accumulation of evidence shows that endogenous neural stem/progenitor cells (NSPCs) are activated following brain injury such as that suffered during ischemic stroke. To understand the expression patterns of these cells, researchers have developed mice that express an NSPC marker, Nestin, which is detectable by specific reporters such as green fluorescent protein (GFP), i.e., Nestin-GFP mice. However, the genetic background of most transgenic mice, including Nestin-GFP mice, comes from the C57BL/6 strain. Because mice from this background strain have many cerebral arterial branches and coll

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Fattman, Cheryl L., Federica Gambelli, Gary Hoyle, Bruce R. Pitt, and Luis A. Ortiz. "Epithelial expression of TIMP-1 does not alter sensitivity to bleomycin-induced lung injury in C57BL/6 mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 3 (2008): L572—L581. http://dx.doi.org/10.1152/ajplung.00291.2007.

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Matrix metalloproteinases (MMPs) are mediators of lung injury, and their activity has been associated with the development of pulmonary fibrosis. To understand how MMPs regulate the development of pulmonary fibrosis, we examined MMP expression in two strains of mice with differing sensitivities to the fibrosis-inducing drug bleomycin. After a single intratracheal injection of the drug, bleomycin-sensitive C57BL/6 mice showed increased expression for MMPs (-2, -7, -9, -13) at both 7 and 14 days posttreatment compared with the bleomycin-resistant BALB/c strain. In addition, TIMP-1, an endogenous

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Kajiwara, Hideko, Mitsumasa Saito, Shouichi Ohga, Takeshi Uenotsuchi, and Shin-ichi Yoshida. "Impaired Host Defense against Sporothrix schenckii in Mice with Chronic Granulomatous Disease." Infection and Immunity 72, no. 9 (2004): 5073–79. http://dx.doi.org/10.1128/iai.72.9.5073-5079.2004.

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ABSTRACT We compared the immune defense of mice with chronic granulomatous disease (CGD mice) with that of wild-type C57BL/6 mice for their response to Sporothrix schenckii. A subcutaneous injection of 5 × 104 CFU S. schenckii strain IFM41598 into CGD mice resulted in systemic infection and death within 84 days. In contrast, injected C57BL/6 mice did not develop systemic infection and were able to survive through 100 days of observation. Differences in host resistance were analyzed in vitro. Neutrophils and macrophages obtained from CGD mice were found to allow greater growth of this organism

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Kimeswenger, Susanne, Barbara Sterniczky, Anne Kramer, et al. "Impact of infrared radiation on UVB-induced skin tumourigenesis in wild type C57BL/6 mice." Photochemical & Photobiological Sciences 18, no. 1 (2019): 129–39. http://dx.doi.org/10.1039/c8pp00118a.

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Zeytun, Ahmet, Mitzi Nagarkatti, and Prakash S. Nagarkatti. "Growth of FasL-bearing tumor cells in syngeneic murine host induces apoptosis and toxicity in Fas+ organs." Blood 95, no. 6 (2000): 2111–17. http://dx.doi.org/10.1182/blood.v95.6.2111.

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Abstract In the current study, we investigated whether the growth of FasL-bearing tumor cells would induce apoptosis and toxicity in organs that express high level of Fas. Sera from C57BL/6 +/+(wild-type) mice injected with syngeneic FasL+ tumors, LSA, or EL-4, showed significantly higher levels of soluble FasL than that from the nontumor-bearing mice. Furthermore, the soluble FasL was functional inasmuch as the sera from tumor-bearing mice were able to induce apoptosis in Fas+ but not Fas−targets. Histopathologic studies and in situ TUNEL assay to detect apoptosis were carried out in C57BL/6

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Fengler, Vera H., Tanja Macheiner, Walter Goessler, Maria Ratzer, Johannes Haybaeck, and Karine Sargsyan. "Hepatic Response of Magnesium-Restricted Wild Type Mice." Metabolites 11, no. 11 (2021): 762. http://dx.doi.org/10.3390/metabo11110762.

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Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice by feeding a magnesium-deficient-diet. Metabolic markers as well as markers of inflammation and liver function were assessed. Furthermore, liver tissue was examined histopathologically and compared with specimens from high-fat-diet fed and control mice. Finally, the

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Tripathi, Deepak, Sambasivan Venkatasubramanian, Satyanarayana Cheekatla, et al. "CD4+CD25+Foxp3+ cells from JNK-/- mice prolong pancreatic allograft survival in type 1 diabetic mice (TRAN2P.970)." Journal of Immunology 194, no. 1_Supplement (2015): 209.10. http://dx.doi.org/10.4049/jimmunol.194.supp.209.10.

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Abstract In the current study we asked whether modified CD4+CD25+FoxP3+ regulatory T-cells (T-regs) can induce long term allograft tolerance. Pancreatic islets from BALB/c mice survived in a type 1 diabetic C57BL/6 mice (recipient mice) liver up to 18-21 days (n=5). Preloading islets with T-regs from WT (wild type) C57BL/6 mice, enhanced survival up to 37 days (N=5 and p = 0.003). Further preloading islets with T-regs from JNK1-/- mice (C57BL/6 background) enhanced survival up to 107 days (N=5 and p = 0.002). In contrast preloading islets with T-regs from FAS-/- (C57BL/6 background) did not en

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Yamato, Fumiko, Junji Takaya, Shoji Tsuji, Masafumi Hasui, and Kazunari Kaneko. "Angiotensin Type 1a Receptor Signaling Is Not Necessary for the Production of Reactive Oxygen Species in Polymorphonuclear Leukocytes." ISRN Inflammation 2012 (December 4, 2012): 1–5. http://dx.doi.org/10.5402/2012/347852.

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Background. Although angiotensin II (Ang II) has inflammatory effects, little is known about its role in polymorphonuclear leucocytes (PMLs). To elucidate the role of Ang II in PMLs ROS production, we examined hydrogen peroxide (H2O2), one of the ROS, and NO production in AT1a receptor knockout (AT1KO) mice. Methods and Results. PMLs were analyzed from Ang II type 1a receptor knockout mice (AT1KO) and C57BL/6 wild type mice. Using flow cytometry, we studied hydrogen peroxide (H2O2) production from PMLs after Staphylococcus aureus phagocytosis or phorbol myristate acetate (PMA) stimulation. Nit

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li, heng, Qiongwen Wu, Lei Guo, et al. "URT bacterial microbiota interacted with H1N1 infection by IL-1 pathway in C57BL/6." Journal of Immunology 202, no. 1_Supplement (2019): 120.17. http://dx.doi.org/10.4049/jimmunol.202.supp.120.17.

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Abstract The bacterial microbiota correlated with the inflammatory response, and inflammations are developed with high frequency when infections happened in the upper respiratory tract (URT). However, it has rarely been studied that the mechanisms in the interaction between the bacterial microbiota and the infections appeared in URT. In our subjects, we researched the interaction between H1N1 infection and URT bacterial microbiota by IL-1 pathway in C57BL/6. We extracted the DNA in URT and performed 16S rRNA amplicon sequencing. When IL1 gene was knocked out, Streptococcus, Bergeyella and Ente

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Fox, JG, X. Li, RJ Cahill, et al. "Hypertrophic gastropathy in Helicobacter felis-infected wild-type C57BL/6 mice and p53 hemizygous transgenic mice." Gastroenterology 110, no. 1 (1996): 155–66. http://dx.doi.org/10.1053/gast.1996.v110.pm8536852.

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Breitbach, Katrin, Sonja Klocke, Thomas Tschernig, Nico van Rooijen, Ulrich Baumann, and Ivo Steinmetz. "Role of Inducible Nitric Oxide Synthase and NADPH Oxidase in Early Control of Burkholderia pseudomallei Infection in Mice." Infection and Immunity 74, no. 11 (2006): 6300–6309. http://dx.doi.org/10.1128/iai.00966-06.

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ABSTRACT Infection with the soil bacterium Burkholderia pseudomallei can result in a variety of clinical outcomes, including asymptomatic infection. The initial immune defense mechanisms which might contribute to the various outcomes after environmental contact with B. pseudomallei are largely unknown. We have previously shown that relatively resistant C57BL/6 mice can restrict bacterial B. pseudomallei growth more efficiently within 1 day after infection than highly susceptible BALB/c mice. By using this model, our study aimed to investigate the role of macrophage-mediated effector mechanisms

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Desroches-Castan, Agnès, Emmanuelle Tillet, Nicolas Ricard, et al. "Differential Consequences of Bmp9 Deletion on Sinusoidal Endothelial Cell Differentiation and Liver Fibrosis in 129/Ola and C57BL/6 Mice." Cells 8, no. 9 (2019): 1079. http://dx.doi.org/10.3390/cells8091079.

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The aim of the present work was to address the role of BMP9 in different genetic backgrounds (C57BL/6, BALB/c, and 129/Ola) of mice deleted for Bmp9. We found that Bmp9 deletion led to premature mortality only in the 129/Ola strain. We have previously shown that Bmp9 deletion led to liver sinusoidal endothelial cells (LSEC) capillarization and liver fibrosis in the 129/Ola background. Here, we showed that this is not the case in the C57BL/6 background. Analysis of LSEC from Wild-type (WT) versus Bmp9-KO mice in the C57BL/6 background showed no difference in LSEC fenestration and in the express

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Yonekura, Ichiro, Nobutaka Kawahara, Hirofumi Nakatomi, Kazuhide Furuya, and Takaaki Kirino. "A Model of Global Cerebral Ischemia in C57 BL/6 Mice." Journal of Cerebral Blood Flow & Metabolism 24, no. 2 (2004): 151–58. http://dx.doi.org/10.1097/01.wcb.0000096063.84070.c1.

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A reproducible model of global cerebral ischemia in mice is essential for elucidating the molecular mechanism of ischemic neuronal injury. Such a model is particularly important in the mouse because many genetically engineered mutant animals are available. In C57BL/6 and SV129/EMS mice, we evaluated a three-vessel occlusion model. Occlusion of the basilar artery with a miniature clip was followed by bilateral carotid occlusion. The mean cortical cerebral blood flow was reduced to less than 10% of the preischemic value, and the mean anoxic depolarization was attained within 1 minute. In C57BL/6

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Lu, Wenbin, Genshan Ma, Zulong Sheng, et al. "MSCs Contribute to the Conversion of Ly6Chigh Monocytes into Ly6Clow Subsets under AMI." Stem Cells International 2020 (January 13, 2020): 1–10. http://dx.doi.org/10.1155/2020/2460158.

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Background. Ly6Chigh monocytes are inflammatory cells that accumulate in an infarcted myocardium, and Ly6Clow monocytes are believed to be reparative and curb myocardial remodeling. NR4A1 is a novel target for modulating the inflammatory phenotype of monocytes during atherogenesis. Objectives. We aimed to investigate whether MSCs can contribute to the heterogeneity of Ly6Chigh monocytes differentiated into Ly6Clow monocytes and whether this regulation is related to nuclear receptor NR4A1. Methods. Ly6Chigh/low monocytes were first cocultured with MSCs. C57BL/6CX3CR1-/- mice and C57BL/6 wild-ty

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Gorrell, Rebecca J., Odilia L. C. Wijburg, John S. Pedersen, et al. "Contribution of Secretory Antibodies to Intestinal Mucosal Immunity against Helicobacter pylori." Infection and Immunity 81, no. 10 (2013): 3880–93. http://dx.doi.org/10.1128/iai.01424-12.

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ABSTRACTThe natural immune response toHelicobacter pylorineither clears infection nor prevents reinfection. However, the ability of secretory antibodies to influence the course ofH. pyloriinfection has not been determined. We compared the natural progression ofH. pyloriinfection in wild-type C57BL/6 mice with that in mice lacking the polymeric immunoglobulin receptor (pIgR) that is essential for the secretion of polymeric antibody across mucosal surfaces.H. pyloriSS1-infected wild-type and pIgR knockout (KO) mice were sampled longitudinally for gastrointestinal bacterial load, antibody respons

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Lukic, Miodrag L., Allen Shahin, Eric Mensah-Brown, and Ahmed Al-Hakim. "Il-23 enhances diabetes induction in the wild type but not in INF-gamma −/− mice (129.36)." Journal of Immunology 178, no. 1_Supplement (2007): S224. http://dx.doi.org/10.4049/jimmunol.178.supp.129.36.

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Abstract C57BL/6 male mice developed delayed progressive and sustained hyperglucemia, insulitis and loss of β cells when injected with 5 (40 μg/ kg b/w) daily doses of streptozotocin (STZ). C57BL/6 INF-γ −/− mice treated with same regimen develop the disease at the later stage (by day 28) but reach the same level of functional impairment by day 52 after disease induction. RT PCR analysis of the pancreatic lymph nodes revealed the presence of TNF, INF-γ, and IL-17 and in the “wild type” mice and only TNF-α and IL-17 in INF-γ −/− mice. Four injections of STZ did not induce hyperglycemia neither

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Tu, Xiaolong, Xinhe Feng, Weifang Wang, et al. "Abstract 7174: Pharmacokinetics and immunogenicity of anti-PD-1 antibody in humanized FcRn mouse models compared to immunocompetent mouse models." Cancer Research 84, no. 6_Supplement (2024): 7174. http://dx.doi.org/10.1158/1538-7445.am2024-7174.

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Abstract Introduction: The development and use of therapeutic antibodies in cancer therapy has increased significantly in recent years, led by the success of approved immune checkpoint blockade antibodies targeting PD-1 and PD-L1 axis. However, obtaining more clinically relevant pharmacokinetics (PK), safety and efficacy data for antibodies is still challenging in preclinical phase. Humanized FcRn (hFcRn) transgenic mouse model has a more faithful catabolism compared to WT mice, providing more accurate and predictable PK data of innovative antibody-based therapeutics at discovery stage[1]. In

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