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C57BL6 Mice (c57bl6 + mouse)
Selected AbstractsIsoflurane attenuates pulmonary interleukin-1, and systemic tumor necrosis factor-, following mechanical ventilation in healthy miceACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009M. VANEKER Background: Mechanical ventilation (MV) induces an inflammatory response in healthy lungs. The resulting pro-inflammatory state is a risk factor for ventilator-induced lung injury and peripheral organ dysfunction. Isoflurane is known to have protective immunological effects on different organ systems. We tested the hypothesis that the MV-induced inflammatory response in healthy lungs is reduced by isoflurane. Methods: Healthy C57BL6 mice (n=34) were mechanically ventilated (tidal volume, 8 ml/kg; positive end-expiratory pressure, 4 cmH2O; and fraction of inspired oxygen, 0.4) for 4 h under general anesthesia using a mix of ketamine, medetomidine and atropine (KMA). Animals were divided into four groups: (1) Unventilated control group; (2) MV group using KMA anesthesia; (3) MV group using KMA with 0.25 MAC isoflurane; (4) MV group using KMA with 0.75 MAC isoflurane. Cytokine levels were measured in lung homogenate and plasma. Leukocytes were counted in lung tissue. Results: Lung homogenates: MV increased pro-inflammatory cytokines. In mice receiving KMA+ isoflurane 0.75 MAC, no significant increase in interleukin (IL)-1, was found compared with non-ventilated control mice. Plasma: MV induced a systemic pro-inflammatory response. In mice anesthetized with KMA+ isoflurane (both 0.25 and 0.75 MAC), no significant increase in tumor necrosis factor (TNF)-, was found compared with non-ventilated control mice. Conclusions: The present study is the first to show that isoflurane attenuates the pulmonary IL-1, and systemic TNF-, response following MV in healthy mice. [source] Vaccination with ,-Irradiated Neospora caninum Tachyzoites Protects Mice Against Acute Challenge with N. caninumTHE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 2 2006S. RAMAMOORTHY ABSTRACT. Neospora caninum, an apicomplexan parasite, is a leading cause of bovine abortions worldwide. The efficacy of ,-irradiated N. caninum strain NC-1 tachyzoites as a vaccine for neosporosis was assessed in C57BL6 mice. A dose of 528 Gy of , irradiation was sufficient to arrest replication but not host cell penetration by tachyzoites. Female C57BL6 mice were vaccinated with two intraperitoneal inoculations of 1 × 106 irradiated tachyzoites at 4-wk intervals. When stimulated with N. caninum tachyzoite lysates, splenocytes of vaccinated mice, cultured 5 and 10 wk after vaccination, secreted significant (P<0.05) levels of interferon ,, interleukin (IL)-10, and small amounts of IL-4. Antibody isotype-specific ELISA of sera from vaccinated mice exhibited both IgG1 and IgG2a isotypes of antibodies. Vaccinated mice were challenged intraperitoneally with 2 × 107N. caninum tachyzoites. All vaccinated mice remained healthy and showed no obvious signs of neosporosis up to the 25th day post-challenge when the study was terminated. All unvaccinated control mice died within 1 wk of infection. Gamma-irradiated N. caninum tachyzoites can serve as an effective, attenuated vaccine for N. caninum. [source] Delayed neovascularization in inflammation-induced corneal neovascularization in interleukin-10-deficient miceACTA OPHTHALMOLOGICA, Issue 2 2010Branka Samolov Abstract. Purpose:, To investigate the potential modulatory role of interleukin-10 (IL-10) in the suture model for corneal neovascularization. Methods:, Neovascularized areas were measured on corneal flat-mounts in IL-10,/, and wild-type C57BL6 mice. The inflammatory cellular response was characterized with immunohistochemistry. Gene expression was measured by real-time polymerase chain reaction. Results:, IL-10,/, mice showed a delayed neovascular response compared to wild-type animals at day 6 after suture, when approximately half of the cornea was neovascularized. No apparent differences in inflammatory responses or in messenger RNA (mRNA) expression for proangiogenic factors were detected in IL-10,/, versus wild-type mice. Conclusion:, IL-10 appears to have a proangiogenic effect in the suture model for corneal neovascularization that cannot be explained by either IL-10's anti-inflammatory effect or apparent cross-talk with the angiogenic factors vascular endothelial growth factor (VEGF)-A, metalloproteinase (MMP)-2 and MMP-9, angiopoietin (Ang)-1 and Ang-2. [source] Lack of effect of gender on retinopathy in the mouseCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 5 2001Rosemary D Higgins MD ABSTRACT Background: The reported effect of gender on retinopathy of prematurity has been controversial. The goal of this study was to determine the effect of gender on oxygen-induced retinopathy in a mouse model. Methods: Oxygen-induced retinopathy was produced in C57BL6 mice by exposure to 75% oxygen from postnatal day (P) 7 for 5 days. Animals were returned to room air on P12 and killed on P17,21. Gender was determined by inspection. Retinopathy was evaluated by a retinopathy scoring system and by quantification of extraretinal neovascular nuclei on retinal sections. Results: Both males and females developed similar degrees of retinopathy. Males had a median total retinopathy score of 9 (25th, 75th quartile: 8, 11) and females had score of 9 (25th, 75th quartile: 7,10). Retinal subscores of blood vessel growth, blood vessel tufts, extraretinal neovascularization, haemorrhage and blood vessel tortuosity were similar in both groups. Males and females had a similar number of neovascular nuclei on retinal sections. Conclusions: Gender does not alter the development of oxygen-induced retinopathy in the C57BL6 mouse. [source] DNA damage response and cellular senescence in tissues of aging miceAGING CELL, Issue 3 2009Chunfang Wang Summary The impact of cellular senescence onto aging of organisms is not fully clear, not at least because of the scarcity of reliable data on the mere frequency of senescent cells in aging tissues. Activation of a DNA damage response including formation of DNA damage foci containing activated H2A.X (,-H2A.X) at either uncapped telomeres or persistent DNA strand breaks is the major trigger of cell senescence. Therefore, ,-H2A.X immunohistochemistry (IHC) was established by us as a reliable quantitative indicator of senescence in fibroblasts in vitro and in hepatocytes in vivo and the age dependency of DNA damage foci accumulation in ten organs of C57Bl6 mice was analysed over an age range from 12 to 42 months. There were significant increases with age in the frequency of foci-containing cells in lung, spleen, dermis, liver and gut epithelium. In liver, foci-positive cells were preferentially found in the centrilobular area, which is exposed to higher levels of oxidative stress. Foci formation in the intestine was restricted to the crypts. It was not associated with either apoptosis or hyperproliferation. That telomeres shortened with age in both crypt and villus enterocytes, but telomeres in the crypt epithelium were longer than those in villi at all ages were confirmed by us. Still, there was no more than random co-localization between ,-H2A.X foci and telomeres even in crypts from very old mice, indicating that senescence in the crypt enterocytes is telomere independent. The results suggest that stress-dependent cell senescence could play a causal role for aging of mice. [source] Development of layer-specific axonal arborizations in mouse primary somatosensory cortexTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 3 2006DeLaine D. Larsen Abstract In the developing neocortex, pyramidal neurons use molecular cues to form axonal arbors selectively in the correct layers. Despite the utility of mice for molecular and genetic studies, little work has been done on the development of layer-specific axonal arborizations of pyramidal neurons in mice. We intracellularly labeled and reconstructed the axons of layer 2/3 and layer 5 pyramidal neurons in slices of primary somatosensory cortex from C57Bl6 mice on postnatal days 7,21. For all neurons studied, the development of the axonal arborizations in mice follows a pattern similar to that seen in other species; laminar specificity of the earliest axonal branches is similar to that of mature animals. At P7, pyramidal neurons are very simple, having only a main descending axon and few primary branches. Between P7 and P10, there is a large increase in the total number of axonal branches, and axons continue to increase in complexity and total length from P10 to P21. Unlike observations in ferrets, cats, and monkeys, two types of layer 2/3 pyramidal neurons are present in both mature and developing mice; cells in superficial layer 2/3 lack axonal arbors in layer 4, and cells close to the layer 4 border have substantial axonal arbors within layer 4. We also describe axonal and dendritic arborization patterns of three pyramidal cell types in layer 5. The axons of tall-tufted layer 5 pyramidal neurons arborize almost exclusively within deep layers while tall-simple, and short layer 5 pyramidal neurons also project axons to superficial layers. J. Comp. Neurol. 494:398,414, 2006. © 2005 Wiley-Liss, Inc. [source] Gene transfer of disease regulated promoters during experimental autoimmune uveitisACTA OPHTHALMOLOGICA, Issue 2009V ELMALEH Purpose Adeno-associated virus (AAV) vectors have been successfully used to transfer immunosuppressive genes into the retina to prevent experimental uveitis development. Transgene expression is classically regulated by constitutive or tetracycline inducible promoters. It might be more advantageous that the control of transgene expression depends on the pathological process itself. Inflammation activates transcription factors acting on promoters containing short responsive sequences, responding, for example to nuclear factor kappa B (NF,B-RE). These responsive elements can be used to generate disease regulated promoters. Methods An AAV vector with the GFP gene under the control of a NF-kB-RE containing promoter will be injected subretinally in C57Bl6 mice. Autoimmune uveitis will be induced by adoptive transfer of IRBP specific lymphocytes. Animals will be sacrificed at different time points. GFP expression will be analysed by immunofluorescence. VCAM1, MHC II and CD45 will be analysed by immunofluorescence and used to monitor the level of retinal inflammation. Results One week after disease induction, GFP expression was found in eyes injected with this new vector. Milder GFP expression was also found in mice who did not received adoptive transfer. This background was increased a J14. Conclusion Our preliminary results suggest that disease driven GFP expression can be obtained by the use of AAV vectors containing disease regulated promoters. We still need some more times to improve our model. In the future, we plan to replace the GFP gene by an immunosuppressive gene and test if the system can be use to treat experimental uveitis. [source] | |||||||||||||