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1.
The effect of enhanced green fluorescent protein (EGFP) on the in vitro viability of early embryos of C57BL/6--Tgn(ACTbEGFP010sb/J mice has been studied. The number of viable ova in hemizygous females (-/egfp) has been shown to decrease. Irrespective of the EGFP level, it has no deleterious effect on the early development of embryos obtained by reciprocal crossing of hemizygous (-/egfp) and wild-type (-/-) mice. 相似文献
2.
Gastric Pit Cell Hyperplasia and Glandular Atrophy in Carbonic Anhydrase IX Knockout Mice: Studies on Two Strains C57/BL6 and BALB/C 总被引:1,自引:0,他引:1
Leppilampi M Karttunen TJ Kivelä J Gut MO Pastoreková S Pastorek J Parkkila S 《Transgenic research》2005,14(5):655-663
Carbonic anhydrase (CA) isoenzyme IX is a hypoxia-inducible enzyme, which is expressed in the human and rodent gastrointestinal
tract and overexpressed in several different tumors. Functionally, it has probably an effect on proliferation and differentiation
of gastrointestinal epithelial cells. It may also participate in gastric morphogenesis, since a recent study has shown gastric
pit cell hyperplasia and glandular atrophy in CA IX-knockout mice. However, it is not known whether CA IX produces morphological
changes in the gastric mucosa, which can turn into a dysplasia or malignancy in the presence of some carcinogenic factors.
High-salt diet is considered such a factor which has been shown to modulate Helicobacter pylori-associated carcinogenesis. We produced two strains of CA IX-knockout mice, C57/BL6 and BALB/c, and the mice ate either standard
or high-salt feed for 20 weeks. Stomach samples were collected from 40 Car9−/− knockout mice and 37 wildtype littermates, and the tissue sections were examined for histology. CA IX-deficiency caused gastric
pit cell hyperplasia and glandular atrophy in both BALB/c and C57/BL6 strains. Excess dietary salt had no significant effect
on the severity of pit cell hyperplasia. No dysplasia was found in any of the groups. In C57/BL6 mice, CA IX-deficiency was
associated with gastric submucosal inflammation. The results indicate that CA IX-deficiency provides a useful model to study
the mechanisms of gastric morphogenesis and epithelial integrity. Further studies are needed to see whether CA IX has a role
in the regulation of immune response. The findings suggest that although CA IX-deficiency is not a tumor-promoting factor
per se, it induces glandular atrophy in the body mucosa, a lesion which is considered to be a preneoplastic alteration in the stomach. 相似文献
3.
Manjul Dutt Dong H. Lee Jude W. Grosser 《In vitro cellular & developmental biology. Plant》2010,46(6):467-476
Agrobacterium-mediated transformation of Carrizo citrange [Citrus sinensis (L.) Osbeck × Poncirus trifoliata (L.) Raf.] with a binary vector containing a novel bifunctional reporter–selection fusion gene comprising an in-frame fusion
between the manA gene and egfp gene is detailed. This system combined the phosphomannose isomerase positive selection system with the ability to monitor
gene expression in a non-destructive manner using EGFP. Transgenic plants stably expressing the EGFP protein were regenerated
following Agrobacterium-mediated transformation using a vector containing this fusion gene. We also obtained comparable transformation efficiencies
when Carrizo explants were transformed using another Agrobacterium strain containing a binary vector with a bifunctional egfp–nptII fusion gene. Regenerating shoots were selected on medium containing 15 g L−1 mannose supplemented with 5 g L−1 sucrose for the manA-based selection or on medium containing 100 mg L−1 kanamycin for the nptII-based selection. Our results indicated that the mannose-based antibiotic-free selection combined with visual identification
of transgenic shoots using EGFP allows for early elimination of escape non-transgenic shoots and can provide a viable alternative
to antibiotic-based selection systems in the genetic transformation of citrus and other crops. 相似文献
4.
Parra J Klein AD Castro J Morales MG Mosqueira M Valencia I Cortés V Rigotti A Zanlungo S 《Biochemical and biophysical research communications》2011,(3):400-406
Niemann–Pick type C (NPC) disease is an autosomal recessive neurovisceral lipid storage disorder. The affected genes are NPC1 and NPC2. Mutations in either gene lead to intracellular cholesterol accumulation. There are three forms of the disease, which are categorized based on the onset and severity of the disease: the infantile form, in which the liver and spleen are severely affected, the juvenile form, in which the liver and brain are affected, and the adult form, which affects the brain. In mice, a spontaneous mutation in the Npc1 gene originated in the BALB/c inbred strain mimics the juvenile form of the disease. To study the influence of genetic background on the expression of NPC disease in mice, we transferred the Npc1 mutation from the BALB/c to C57BL/6J inbred background. We found that C57BL/6J-Npc1−/− mice present with a much more aggressive form of the disease, including a shorter lifespan than BALB/c-Npc1−/− mice. Surprisingly, there was no difference in the amount of cholesterol in the brains of Npc1−/− mice of either mouse strain. However, Npc1−/− mice with the C57BL/6J genetic background showed striking spleen damage with a marked buildup of cholesterol and phospholipids at an early age, which correlated with large foamy cell clusters. In addition, C57BL/6J Npc1−/− mice presented red cell abnormalities and abundant ghost erythrocytes that correlated with a lower hemoglobin concentration. We also found abnormalities in white cells, such as cytoplasmic granulation and neutrophil hypersegmentation that included lymphopenia and atypias. In conclusion, Npc1 deficiency in the C57BL6/J background is associated with spleen, erythrocyte, and immune system abnormalities that lead to a reduced lifespan. 相似文献
5.
Mutations in CHD8 are one of the highest genetic risk factors for autism spectrum disorder. Studies in mice that investigate underlying mechanisms have shown Chd8 haploinsufficient mice display some trait disruptions that mimic clinical phenotypes, although inconsistencies have been reported in some traits across different models on the same strain background. One source of variation across studies may be the impact of Chd8 haploinsufficiency on maternal-offspring interactions. While differences in maternal care as a function of Chd8 genotype have not been studied directly, a previous study showed that pup survival was reduced when reared by Chd8 heterozygous dams compared with wild-type (WT) dams, suggesting altered maternal care as a function of Chd8 genotype. Through systematic observation of the C57BL/6 strain, we first determined the impact of Chd8 haploinsufficiency in the offspring on WT maternal care frequencies across preweaning development. We next determined the impact of maternal Chd8 haploinsufficiency on pup care. Compared with litters with all WT offspring, WT dams exhibited less frequent maternal behaviors toward litters consisting of offspring with mixed Chd8 genotypes, particularly during postnatal week 1. Dam Chd8 haploinsufficiency decreased litter survival and increased active maternal care also during postnatal week 1. Determining the impact of Chd8 haploinsufficiency on early life experiences provides an important foundation for interpreting offspring outcomes and determining mechanisms that underlie heterogeneous phenotypes. 相似文献
6.
Audrey L. Hildebrandt Angelene M. Cantwell Michael C. Rule T. R. King 《Immunogenetics》1999,49(7-8):666-672
The recessive male sterility and histoincompatibility mutation (mshi) arose spontaneously in the standard inbred mouse strain BALB/cBy. In addition to generating sterility in homozygous males,
mshi controls the loss of a minor histocompatibility antigen designated H-mshi. To determine whether the H-mshi antigen normally
expressed by the BALB/cBy strain (H-mshic) is the same as or different from the antigen (H-mshix) expressed by the standard inbred C57BL/6J strain or the wild-derived CAST/Ei and SPRET/Ei strains, animals heterozygous
for the mutant antigen-loss allele (H-mshi
–
) and H-mshi
x
were grafted with tail skin from BALB/cBy mice. The long-term retention of grafts by these hosts indicates that the H-mshi
antigen encoded by the BALB/cBy, C57BL/6J, CAST/Ei, and SPRET/Ei strains is histogenically identical. Conservation of this
minor histocompatibility antigen among these evolutionarily diverse strains suggests that H-mshi encodes a functionally important cellular product(s).
Received: 1 August 1998 / Accepted: 26 October 1998 相似文献
7.
Xingsheng Li Mark B. Cope Maria S. Johnson Daniel L. Smith Jr Tim R. Nagy 《Obesity (Silver Spring, Md.)》2010,18(3):456-462
This study investigated the effects of mild calorie restriction (CR) (5%) on body weight, body composition, energy expenditure, feeding behavior, and locomotor activity in female C57BL/6J mice. Mice were subjected to a 5% reduction of food intake relative to baseline intake of ad libitum (AL) mice for 3 or 4 weeks. In experiment 1, body weight was monitored weekly and body composition (fat and lean mass) was determined at weeks 0, 2, and 4 by dual energy X‐ray absorptiometry. In experiment 2, body weight was measured every 3 days and body composition was determined by quantitative magnetic resonance weekly, and energy expenditure, feeding behavior, and locomotor activity were determined over 3 weeks in a metabolic chamber. At the end of both experiments, CR mice had greater fat mass (P < 0.01) and less lean mass (P < 0.01) compared with AL mice. Total energy expenditure (P < 0.05) and resting energy expenditure (P < 0.05) were significantly decreased in CR mice compared with AL mice over 3 weeks. CR mice ate significantly more food than AL mice immediately following daily food provisioning at 1600 hours (P < 0.01). These findings showed that mild CR caused increased fat mass, decreased lean mass and energy expenditure, and altered feeding behavior in female C57BL/6J mice. Locomotor activity or brown adipose tissue (BAT) thermogenic capacity did not appear to contribute to the decrease in energy expenditure. The increase in fat mass and decrease in lean mass may be a stress response to the uncertainty of food availability. 相似文献
8.
Mathias Jucker Lary C. Walker Hui Kuo Min Tian Donald K. Ingram 《Molecular neurobiology》1994,9(1-3):125-133
The present article reviews findings regarding the age-related occurrence of clusters of unusual granules in the brains of
C57BL/6 (B6) mice and discusses the potential relevance of this phenomenon as a model of specific aspects of brain aging in
humans. The granules occur predominatly in the hippocampus of B6 mice and represent aggregations of fibrillar material that
are mostly associated with astrocytes. The deposits become evident at about 4 to 6 mo of age, and increase markedly in both
number and size thereafter. Similar structures have been observed in adult senescence accelerated mice (SAM) and have been
noted, although very rarely, in older mice from other strains. The deposits appear to manifest dominant genetic heritability.
Heparan sulfate proteoglycan and laminin or related molecules have been identified as components of the granular material.
Although the deposits do not represent senile plaques with β-amyloid deposition, they might mimic the deposition of extracellular
matrix molecules that is thought to be an early event in amyloidogenesis in the aged brain and in Alzheimer's disease. 相似文献
9.
Elisabet Johansson Scott C. Wesselkamper George D. Leikauf Ying Chen 《Biochemical and biophysical research communications》2010,396(2):407-248
In this study we examined the role of the antioxidant glutathione (GSH) in pulmonary susceptibility to ozone toxicity, utilizing GSH deficient C57BL/6J mice that lack the expression of glutamate-cysteine ligase modifier subunit (GCLM). Gclm(−/−) knockout mice had 70% GSH depletion in the lung. Gclm(+/+) wild-type and Gclm(−/−) mice were exposed to either 0.3 ppm ozone or filtered air for 48 h. Ozone-induced lung hyperpermeability, as measured by total protein concentration in bronchoalveolar lavage fluid, was surprisingly lower in Gclm(−/−) mice than in wild-type mice. Lung hyperpermeability did not correlate with the degree of neutrophilia or with inflammatory gene expression. Pulmonary antioxidant response to ozone, assessed by increased mRNA levels of metallothionein 1 and 2, α-tocopherol transporter protein, and solute carrier family 23 member 2 (sodium-dependent vitamin C transporter) was greater in Gclm(−/−) mice than in Gclm(+/+) mice. These results suggest that compensatory augmentation of antioxidant defenses in Gclm(−/−) mice may confer increased resistance to ozone-induced lung injury. 相似文献
10.
Wesley G. Beamer Kathryn L. Shultz Gary A. Churchill Wayne N. Frankel David J. Baylink Clifford J. Rosen Leah Rae Donahue 《Mammalian genome》1999,10(11):1043-1049
Genetic analyses for loci regulating bone mineral density have been conducted in a cohort of F2 mice derived from intercross matings of (C57BL/6J × CAST/EiJ)F1 parents. Femurs were isolated from 714 4-month-old females when peak adult bone density had been achieved. Bone mineral density
(BMD) data were obtained by peripheral quantitative computed tomography (pQCT), and genotype data were obtained by Polymerase
Chain Reaction (PCR) assays for polymorphic markers carried in genomic DNA of each mouse. Genome-wide scans for co-segregation
of genetic marker data with high or low BMD revealed loci on eight different chromosomes, four of which (Chrs 1, 5, 13, and
15) achieved conservative statistical criteria for suggestive, significant, or highly significant linkage with BMD. These
four quantitative trait loci (QTLs) were confirmed by a linear regression model developed to describe the main effects; none
of the loci exhibited significant interaction effects by ANOVA. The four QTLs have been named Bmd1 (Chr 1), Bmd2 (Chr 5), Bmd3 (Chr 13), and Bmd4 (Chr 15). Additive effects were observed for Bmd1, recessive for Bmd3, and dominant effects for Bmd2 and Bmd4. The current large size of the QTL regions (6→31 cM) renders premature any discussion of candidate genes at this time. Fine
mapping of these QTLs is in progress to refine their genetic positions and to evaluate human homologies.
Received: 5 May 1999 / Accepted: 22 June 1999 相似文献
11.
Superovulation is a reproductive technique generally used to produce genetically engineered mice. Superovulation in mice involves the administration of equine chorionic gonadotropin (eCG) to promote follicle growth and then that of human chorionic gonadotropin (hCG) to induce ovulation. Previously, some published studies reported that inhibin antiserum (IAS) increased the number of ovulated oocytes in ddY and wild-derived strains of mice. However, the effect of IAS on the C57BL/6 strain, which is the most widely used inbred strain for the production of genetically engineered mice, has not been investigated. In addition, the combined effect of IAS and eCG (IASe) on the number of ovulated oocytes in superovulation treatment has not been examined. In this study, we examined the effect of IAS and eCG on the number of ovulated oocytes in immature female mice of the C57BL/6 strain in superovulation treatment. Furthermore, we evaluated the quality of obtained oocytes produced by superovulation using IASe by in vitro fertilization (IVF) with sperm from C57BL/6 or genetically engineered mice. The developmental ability of fresh or cryopreserved embryos was examined by embryo transfer. The administration of IAS or eCG had a similar effect on the number of ovulated oocytes in C57BL/6 female mice. The number of ovulated oocytes increased to about 3-fold by the administration of IASe than by the administration of IAS or eCG alone. Oocytes derived from superovulation using IASe normally developed into 2-cell embryos by IVF using sperm from C57BL/6 mice. Fresh or cryopreserved 2-cell embryos produced by IVF between oocytes of C57BL/6 mice and sperm from genetically engineered mice normally developed into live pups following embryo transfer. In summary, a novel technique of superovulation using IASe is extremely useful for producing a great number of oocytes and offspring from genetically engineered mice. 相似文献
12.
V. Zermeo S. Espindola E. Mendoza E. Hernndez-Echeagaray 《International journal of biological sciences》2009,5(2):118-127
Neurotrophin expression in early stages of development is crucial for brain assembly and function. In particular, postnatal expression of neurotrophins has not been well documented in the neostriatum and in general neurotrophins or their receptor mRNA's are normally reported, but not protein expression. In the present study, immunocytochemical expression of BDNF, NT-3 and NT-4/5 was characterized in striatal tissue of C57BL/6 mice at postnatal days 10th (P10), 21st (P21), 42nd (P42) and 80th (P80). 相似文献
13.
Effects of FVB/NJ and C57Bl/6J strain backgrounds on mammary tumor phenotype in inducible nitric oxide synthase deficient mice 总被引:3,自引:0,他引:3
Davie SA Maglione JE Manner CK Young D Cardiff RD MacLeod CL Ellies LG 《Transgenic research》2007,16(2):193-201
The ability to genetically manipulate mice has led to rapid progress in our understanding of the roles of different gene products
in human disease. Transgenic mice have often been created in the FVB/NJ (FVB) strain due to its high fecundity, while gene-targeted
mice have been developed in the 129/SvJ-C57Bl/6J strains due to the capacity of 129/SvJ embryonic stem cells to facilitate
germline transmission. Gene-targeted mice are commonly backcrossed into the C57Bl/6J (B6) background for comparison with existing
data. Genetic modifiers have been shown to modulate mammary tumor latency in mouse models of breast cancer and it is commonly
known that the FVB strain is susceptible to mammary tumors while the B6 strain is more resistant. Since gene-targeted mice
in the B6 background are frequently bred into the polyomavirus middle T (PyMT) mouse model of breast cancer in the FVB strain,
we have sought to understand the impact of the different genetic backgrounds on the resulting phenotype. We bred mice deficient
in the inducible nitric oxide synthase (iNOS) until they were congenic in the PyMT model in the FVB and B6 strains. Our results
reveal that the large difference in mean tumor latencies in the two backgrounds of 53 and 92 days respectively affect the
ability to discern smaller differences in latency due to the Nos2 genetic mutation. Furthermore, the longer latency in the
B6 strain enables a more detailed analysis of tumor formation indicating that individual tumor development is not stoichastic,
but is initiated in the #1 glands and proceeds in early and late phases. NO production affects tumors that develop early suggesting
an association of iNOS-induced NO with a more aggressive tumor phenotype, consistent with human clinical data positively correlating
iNOS expression with breast cancer progression. An examination of lung metastases, which are significantly reduced in PyMT/iNOS−/− mice compared with PyMT/iNOS+/+ mice only in the B6 background, is concordant with these findings. Our data suggest that PyMT in the B6 background provides
a useful model for the study of inflammation-induced breast cancer. 相似文献
14.
Xiaobin Han Andrea B. Patters Takashi Ito Junichi Azuma Stephen W. Schaffer Russell W. Chesney 《PloS one》2015,10(1)
Diabetic nephropathy is the leading cause of end stage renal disease in the world. Although tremendous efforts have been made, scientists have yet to identify an ideal animal model that can reproduce the characteristics of human diabetic nephropathy. In this study, we hypothesize that taurine insufficiency is a critical risk factor for development of diabetic nephropathy associated with diabetes mellitus. This hypothesis was tested in vivo in TauT heterozygous (TauT
+/-) and homozygous (TauT-/-) knockout in C57BL/6 background mice. We have shown that alteration of the TauT gene (also known as SLC6A6) has a substantial effect on the susceptibility to development of extensive diabetic kidney disease in both TauT
+/- and TauT-/-mouse models of diabetes. These animals developed histological changes characteristic of human diabetic nephropathy that included glomerulosclerosis, nodular lesions, arteriosclerosis, arteriolar dilation, and tubulointerstitial fibrosis. Immunohistochemical staining of molecular markers of smooth muscle actin, CD34, Ki67 and collagen IV further confirmed these observations. Our results demonstrated that both homozygous and heterozygous TauT gene deletion predispose C57BL/6 mice to develop end-stage diabetic kidney disease, which closely replicates the pathological features of diabetic nephropathy in human diabetic patients. 相似文献
15.
Fahim, Mohamed A. Endurance exercise modulatesneuromuscular junction of C57BL/6NNia aging mice. J. Appl. Physiol. 83(1): 59-66, 1997.The effect ofage and endurance exercise on the physiology and morphology ofneuromuscular junctions (NMJ) of gluteus maximus muscle was studied inC57BL/6NNia mice. Mice were exercised, starting at 7 or 25 mo of age,at 28 m/min for 60 min/day, 5 days/wk for 12 wk, on a rodent treadmill.Intracellular recordings of spontaneous miniature endplate potentials(MEPP) and the quantal content of endplate potentials (EPP) wererecorded from NMJ of 10- and 28-mo-old control and exercised mice.Endurance exercise resulted in significant increases in MEPP amplitudes (23%), quantal content, and safety margin, and a significant decrease in MEPP frequency of young mice, with no change in resting membrane potential or membrane capacitance. Three months of endurance exercise resulted in an increase in MEPP frequency (41%) and decreases in MEPPamplitudes (15%), quantal content, and safety margin of old mice.Endurance exercise resulted in significantly larger nerve terminals(24%) in young animals, suggesting functional adaptation. Nerveterminals in exercised 28-mo-old mice were smaller than in thecorresponding control mice, an indication that exercise minimizedage-related nerve terminal elaboration. It is concluded that thedifferent physiological responses of young and old gluteus maximusmuscles to endurance exercise parallel their morphological responses.This suggests that the mouse NMJ undergoes a process of physiologicaland morphological remodeling during aging, and such plasticity could bemodulated differently by endurance exercise. 相似文献
16.
Ye J 《Immunogenetics》2004,56(6):399-404
Four immunoglobulin heavy chain diversity (IGHD) gene subgroups (DFL16, DSP2, DQ52, and DST4) have been identified previously in BALB/c mice. Although the locations of most IGHD genes have been established based on restriction map and Southern blot analysis, a complete mouse IGHD gene locus map at the sequence level is still not available. In addition, a previous restriction fragment length polymorphism study suggested that significant difference in the IGHD gene locus exists between C57BL/6 and BALB/c mice. The author has now analyzed the C57BL/6 mouse genomic data and established a complete map of the IGHD gene locus. All four IGHD subgroups previously identified in BALB/c mice were found to be present in C57BL/6 mice. However, unlike the BALB/c mice, which have at least 13 IGHD genes, the C57BL/6 genome contains only ten IGHD genes, which include one DFL16, six DSP2, one DQ52, and two DST4 genes. There are also differences in the coding regions of the DST4 and DQ52 genes between the two mouse strains. 相似文献
17.
Previous research utilizing the AcB/BcA recombinant congenic strains (RCS) of mice mapped provisional quantitative trait loci
(QTLs) for the psychostimulant effects of nicotine to multiple regions on chromosomes 7, 11, 12, 14, 16, and 17. The current
study was designed to confirm these QTLs in an A/J (A) × C57Bl/6J (B6) F2 cross and a panel of B6.A chromosome substitution
strains (CSS). The panel of B6.A CSS consists of 21 strains, each carrying a different A/J chromosome on a B6 background.
The A × B6 F2, CSS, A, and B6 mice were tested for sensitivity to the effects of nicotine on locomotor activity using a computerized
open-field apparatus. In A × B6 F2 mice two QTLs were identified which confirm those previously observed in the AcB/BcA RCS.
Significant differences in the expression of nicotine-induced activity were associated with loci on chromosome 11 (D11Mit62) and chromosome 16 (D16Mit131) in the A × B6 F2. At the chromosome 11 QTL, an A allele was associated with lower nicotine-induced activity scores relative
to the B6. In contrast, the A allele was associated with greater relative nicotine activity values for the chromosome 16 QTL.
A survey of the CSS panel confirmed the presence of QTLs for nicotine activation on chromosomes 2, 14, 16, and 17 previously
identified in the AcB/BcA RCS. In the informative CSS strains, A alleles were consistently associated with greater nicotine-induced
activity scores compared to the B6. The results of the present study are the first to validate QTLs for sensitivity to the
effects of nicotine across multiple strains of mice. QTLs on chromosomes 2, 11, 14, 16, and 17 were confirmed in CSS and/or
F2 mice. Significantly, the identification of a QTL on chromosome 16 has now been replicated in three crosses derived from
the A and B6 progenitors. 相似文献
18.
Mohammad A. Ilian Barney R. Sparrow Byung-Woo Ryu Daniel P. Selivonchick Henry W. Schaup 《Journal of biochemical and molecular toxicology》1996,11(1):51-56
The activity and level of hepatic pyruvate carboxylase (PC) has been reported to be altered by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment in mice. If alteration in PC level/activity by TCDD influences TCDD toxicity, one would expect to observe an early post-exposure reduction in PC mRNA. To examine the molecular events responsible for the alteration of PC activity in livers of TCDD-treated mice, we designed a synthetic DNA oligonucleotide probe specific for PC mRNA. Northern blot analysis on RNA extracts from hepatic tissue at various times and doses post-TCDD exposure were done. Furthermore, to elucidate the role of the dioxin Ah locus on alterations of PC activity by TCDD, we utilized C57BL/6J (Ahb/b, Ah high TCDD affinity) mice and a congenic (Ahd/d, Ah low TCDD affinity) mouse strain. At 8 days post TCDD treatment, a dose-dependent reduction of hepatic PC mRNA levels was observed in Ahb/b mice. The response, reduction in PC mRNA levels, in the Ahb/b strain was about 10-fold greater than that of comparably exposed congenic Ahd/d mice. These results indicate that previously reported reductions in PC activity/level by TCDD treatment of mice is a consequence of a reduction in PC mRNA levels and that the effect requires a competent Ah receptor. © 1996 John Wiley & Sons, Inc. 相似文献
19.
Kenji Hiromatsu Jun Usami Yoshiyasu Aoki Masahiko Makino Yasunobu Yoshikai 《Microbiology and immunology》1997,41(3):221-227
We reported previously that CD4+ T cells and B cells in mice with retrovirus-induced murine acquired immunodeficiency syndrome (MAIDS) caused by LP-BM5 murine leukemia virus (MuLV) mixtures increased the expression of Fas antigen (Fas) during progression of the disease. However, the contribution of the Fas/Fas ligand (Fas L) system to the pathogenesis of MAIDS remained unknown. Here, we examined the susceptibility of C57BL/6 (B6) lpr/lpr mice, which has been reported to be defective for the expression of Fas, to MAIDS. We found that the Thy 1.2? CD4 T cells and IgK dull B220+ cells, which are characteristic of MAIDS, increased after the inoculation of LP-BM5 MuLV in B6 lpr/lpr mice. B22+ TCR αβ T cells, unique to lupus prone mice, also increased in the B6 lpr/lpr mice after infection. CD4+ B220+ TCR αβ T cells increased profoundly among the B220+ TCR αβ T cells from LP-BM5 MuLV-infected B6 lpr/lpr mice, while the B220+ TCR αβ T cells observed in non-infected B6 lpr/lpr mice were largely of the CD4? CD8? phenotype. A DNA PCR analysis of the LP-BM5 MuLV-infected B6 lpr/lpr mice revealed the genome integration of defective LP-BM5 virus, further confirming that MAIDS is inducible to B6 lpr/lpr mice. LP-BM5 MuLV-infected lpr/lpr mice died within 3 months, while MAIDS-infected B6 +/+ mice usually died within 5 to 6 months, and B6 lpr/lpr mice not infected with LP-BM5 MuLV lived more than 6 months. Taken together, these results suggest that MAIDS is inducible independently with functional Fas expression and the possibility of accelerated progression of murine AIDS and lpr-associated autoimmune disease in B6 lpr/lpr mice infected with LP-BM5 MuLV. 相似文献
20.
【背景】肺部菌群与宿主健康和呼吸道疾病密切相关,耐碳青霉烯类肺炎克雷伯菌(carbapenem-resistantKlebsiella pneumonia,CRKP)是临床常见的条件致病菌,感染后对肺部菌群的影响尚不清楚。【目的】探究耐碳青霉烯类肺炎克雷伯杆菌CRKP2对C57BL/6小鼠肺部菌群的扰动。【方法】将C57BL/6小鼠随机分为3组,分别用CRKP2、碳青霉烯类敏感肺炎克雷伯菌KP2044和无菌PBS溶液滴鼻,利用16S rRNA基因的高通量测序技术分析肺部菌群结构。【结果】与健康小鼠相比,菌株KP2044和CRKP2感染后小鼠肺部菌群α多样性和β多样性均显著改变,变形菌门相对丰度显著增加,乳酸杆菌属相对丰度明显下降。与KP2044相比,CRKP2生物膜形成能力较弱,感染后小鼠死亡率较低,对肺部菌群的扰动较小。【结论】虽然肺炎克雷伯菌是条件致病菌,但高剂量耐碳青霉烯类肺炎克雷伯菌CRKP2仍对健康小鼠肺部菌群造成显著影响;尽管菌株CRKP2具有多重耐药性,但与菌株KP2044相比对肺部菌群的扰动较小,因此推测KP菌株感染对肺部菌群的扰动程度可能与菌株毒力有关。 相似文献