The Experts below are selected from a list of 60 Experts worldwide ranked by ideXlab platform
Samantha Gruenheid - One of the best experts on this subject based on the ideXlab platform.
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The Cri1 locus is the common genetic cause of susceptibility to Citrobacter rodentium infection in C3H and FVB Mouse strains.
Gut Microbes, 2011Co-Authors: Sarah Teatero, Eduardo Diez, Lei Zhu, Danielle Malo, Jenny-lee Thomassin, Samantha GruenheidAbstract:Citrobacter rodentium is a natural pathogen of mice that causes intestinal hyperplasia and colitis. Resistant strains such as C57BL/6J (B6) experience a self-limiting disease that peaks between one and two weeks post infection, followed by a clearing of the infection and complete recovery. However, the inbred Mouse strains C3H/HeJ (C3), C3H/HeOuJ (C3Ou) and FVB/N (FVB) are highly susceptible to C. rodentium infection and develop more severe symptoms of disease leading to high rates of mortality during infection. We have recently demonstrated through a systematic genetics approach that a single locus on proximal chromosome 15 is responsible for the susceptibility of both C3 and C3Ou mice to C. rodentium infection. We have named the locus Citrobacter rodentium infection 1 (Cri1). Here we show that Cri1 also controls susceptibility to C. rodentium in FVB mice, using a targeted method of genotyping to stratify (B6 x FVB)F2 mice according to their genotype at Cri1. Mice that inherit two copies of the resistant...
Dan V Mourich - One of the best experts on this subject based on the ideXlab platform.
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lymphocytic choriomeningitis virus infection in FVB Mouse produces hemorrhagic disease
PLOS Pathogens, 2012Co-Authors: Frederick J Schnell, Sarah Sundholm, Stacy Crumley, Patrick L Iversen, Dan V MourichAbstract:The viral family Arenaviridae includes a number of viruses that can cause hemorrhagic fever in humans. Arenavirus infection often involves multiple organs and can lead to capillary instability, impaired hemostasis, and death. Preclinical testing for development of antiviral or therapeutics is in part hampered due to a lack of an immunologically well-defined rodent model that exhibits similar acute hemorrhagic illness or sequelae compared to the human disease. We have identified the FVB Mouse strain, which succumbs to a hemorrhagic fever-like illness when infected with lymphocytic choriomeningitis virus (LCMV). FVB mice infected with LCMV demonstrate high mortality associated with thrombocytopenia, hepatocellular and splenic necrosis, and cutaneous hemorrhage. Investigation of inflammatory mediators revealed increased IFN-γ, IL-6 and IL-17, along with increased chemokine production, at early times after LCMV infection, which suggests that a viral-induced host immune response is the cause of the pathology. Depletion of T cells at time of infection prevented mortality in all treated animals. Antisense-targeted reduction of IL-17 cytokine responsiveness provided significant protection from hemorrhagic pathology. F1 mice derived from FVB×C57BL/6 mating exhibit disease signs and mortality concomitant with the FVB challenged mice, extending this model to more widely available immunological tools. This report offers a novel animal model for arenavirus research and pre-clinical therapeutic testing.
Sarah Teatero - One of the best experts on this subject based on the ideXlab platform.
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The Cri1 locus is the common genetic cause of susceptibility to Citrobacter rodentium infection in C3H and FVB Mouse strains.
Gut Microbes, 2011Co-Authors: Sarah Teatero, Eduardo Diez, Lei Zhu, Danielle Malo, Jenny-lee Thomassin, Samantha GruenheidAbstract:Citrobacter rodentium is a natural pathogen of mice that causes intestinal hyperplasia and colitis. Resistant strains such as C57BL/6J (B6) experience a self-limiting disease that peaks between one and two weeks post infection, followed by a clearing of the infection and complete recovery. However, the inbred Mouse strains C3H/HeJ (C3), C3H/HeOuJ (C3Ou) and FVB/N (FVB) are highly susceptible to C. rodentium infection and develop more severe symptoms of disease leading to high rates of mortality during infection. We have recently demonstrated through a systematic genetics approach that a single locus on proximal chromosome 15 is responsible for the susceptibility of both C3 and C3Ou mice to C. rodentium infection. We have named the locus Citrobacter rodentium infection 1 (Cri1). Here we show that Cri1 also controls susceptibility to C. rodentium in FVB mice, using a targeted method of genotyping to stratify (B6 x FVB)F2 mice according to their genotype at Cri1. Mice that inherit two copies of the resistant...
Marcela Sorelli Carneiroramos - One of the best experts on this subject based on the ideXlab platform.
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diet induced obesity differentially modulates cardiac inflammatory status in the c57 and FVB Mouse strains
Current Molecular Medicine, 2021Co-Authors: Fernanda Gaislersilva, Carolina Victoria Cruz Junho, Izabelle Fredodacosta, Marcelo A Christoffolete, Marcela Sorelli CarneiroramosAbstract:BACKGROUND Cardiovascular diseases correspond to the highest risk of sudden death worldwide, and obesity is largely related to being an increased risk factor. There is a higher prevalence of arterial hypertension in obese individuals, including the presence of cardiac hypertrophy. METHODS It is already known the role of toll-like receptors [TLR], mainly 2 and 4 in heart cells, as fundamental to the process of cardiac hypertrophy. Obesity has been studied as an activator of damage-associated molecular patterns [DAMPs], which use the TLR signaling pathway to increase the nuclear factor of inflammation, NF-kB, increasing cytokine expression in heart tissue. It's already known that FVB/N and C57BL/6 Mouse strains have different behaviors in relation to metabolism, but the difference in cardiac tropism and innate immune system modulation is not clear. RESULTS The present study aimed to evaluate the contribution of innate immune factors to cardiac hypertrophy induced by an experimental model of obesity comparing two Mouse strains: C57BL/6 and FVB/N. Both strains were submitted to a high-fat diet containing 23% protein, 35.5% carbohydrate, and 35.9% fat for 68 days. Hearts were collected, weighed, and submitted to RT-qPCR, and iBoplex analyzed the serum. We observed an increase in heart mass after 68 days in both strains. CONCLUSION This was followed by an increase of -actin only in C57BL/6 while ANF was increased in FVB/N. Gene expression of innate immune components and inflammatory cytokines were only increased in C57BL/6, but not in FVB/N. Based on the results obtained, we verified that C57BL/6 mice had a more robust action of innate immune system than FVB/N.
Paul N Epstein - One of the best experts on this subject based on the ideXlab platform.
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FVB Mouse genotype confers susceptibility to ove26 diabetic albuminuria
American Journal of Physiology-renal Physiology, 2010Co-Authors: Yun Huang, Shirong Zheng, Paul N EpsteinAbstract:OVE26 (OVE) diabetic mice on the inbred strain FVB are a valuable model of diabetic nephropathy that excretes the highest amount of urine albumin of all diabetic Mouse models. Crossing of OVE mice to C57BL6 or DBA2 mice reduced albuminuria 17-fold in F1 diabetic offspring without reducing diabetes. When comparing renal histology of OVE mice on the FVB background to F1 C57BL6 crosses, we found that the F1 kidneys had significantly smaller glomeruli, much less albumin accumulation in tubules, reduced mesangial matrix expansion, and less interstitial fibrosis. A genome scan of 108 OVE-positive N2 offspring for albuminuria revealed one significant peak on chromosome 11 and nearly significant peaks on chromosomes 9, 13, and 19. Homozygosity for the FVB genotype for peaks on chromosomes 11, 13, or 19 increased albuminuria. Homozygosity for the chromosome 9 peak reduced albuminuria. Combined homozyogosity for the peaks on chromosomes 11, 13, and 19 increased albuminuria over 12-fold and accounted for >70% of the difference between OVE mice on the FVB vs. the F1 background. These loci contain sequences important to susceptibility to diabetic albuminuria.
