Infection of inbred strains of mice with Sendai virus

1978 ◽  
Vol 24 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Robert B. Stewart ◽  
M. Jane Tucker
Keyword(s):  
Sendai Virus ◽  
Inbred Strains ◽  
Virus Growth ◽  
Inbred Strains Of Mice ◽  
Mouse Tissues ◽  
Antiviral Antibody ◽  
In Vivo Growth ◽  
Significant Mortality

A comparative study of the consequences of Parainfluenza type 1 (Sendai) virus infection in inbred (C57B1/6J, C57Br, CBA, DBA) strains and a randomly bred (Swiss white) strain of mice showed significant mortality in the inbred strains but not in the randomly bred ones. This difference may be partly related to the high levels of virus growth obtained in the lungs of the inbred strains contrasted to little or no virus growth in the lungs of the Swiss white mice. A similar difference between these mice was found in the incidence of virus involvement of a variety of mouse tissues. These differences in mortality and in vivo growth of virus were not clearly mimicked in antiviral-antibody production in these different mouse populations.

Effect of murine strain on metabolic pathways of glucose production after brief or prolonged fasting

2005 ◽  
Vol 289 (1) ◽  
pp. E53-E61 ◽  
Author(s):  
Shawn C. Burgess ◽  
F. Mark H. Jeffrey ◽  
Charles Storey ◽  
Angela Milde ◽  
Natasha Hausler ◽  
...  
Keyword(s):  
Genetic Manipulation ◽  
Glucose Production ◽  
Tca Cycle ◽  
Inbred Strains ◽  
Mouse Strains ◽  
Background Strain ◽  
Metabolic Fluxes ◽  
Inbred Strains Of Mice ◽  
Total Glucose

Background strain is known to influence the way a genetic manipulation affects mouse phenotypes. Despite data that demonstrate variations in the primary phenotype of basic inbred strains of mice, there is limited data available about specific metabolic fluxes in vivo that may be responsible for the differences in strain phenotypes. In this study, a simple stable isotope tracer/NMR spectroscopic protocol has been used to compare metabolic fluxes in ICR, FVB/N (FVB), C57BL/6J (B6), and 129S1/SvImJ (129) mouse strains. After a short-term fast in these mice, there were no detectable differences in the pathway fluxes that contribute to glucose synthesis. However, after a 24-h fast, B6 mice retain some residual glycogenolysis compared with other strains. FVB mice also had a 30% higher in vivo phospho enolpyruvate carboxykinase flux and total glucose production from the level of the TCA cycle compared with B6 and 129 strains, while total body glucose production in the 129 strain was ∼30% lower than in either FVB or B6 mice. These data indicate that there are inherent differences in several pathways involving glucose metabolism of inbred strains of mice that may contribute to a phenotype after genetic manipulation in these animals. The techniques used here are amenable to use as a secondary or tertiary tool for studying mouse models with disruptions of intermediary metabolism.

Examining basal chloride transport using the nasal potential difference response in a murine model

2001 ◽  
Vol 281 (5) ◽  
pp. L1173-L1179 ◽  
Author(s):  
Kristine G. Brady ◽  
Thomas J. Kelley ◽  
Mitchell L. Drumm
Keyword(s):  
Cystic Fibrosis ◽  
Chloride Transport ◽  
Inbred Mice ◽  
Inbred Strains ◽  
Potential Difference ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Inbred Strains Of Mice ◽  
Cystic Fibrosis Transmembrane

Epithelia of humans and mice with cystic fibrosis are unable to secrete chloride in response to a chloride gradient or to cAMP-elevating agents. Bioelectrical properties measured using the nasal transepithelial potential difference (TEPD) assay are believed to reflect these cystic fibrosis transmembrane conductance regulator (CFTR)-dependent chloride transport defects. Although the response to forskolin is CFTR mediated, the mechanisms responsible for the response to a chloride gradient are unknown. TEPD measurements performed on inbred mice were used to compare the responses to low chloride and forskolin in vivo. Both responses show little correlation between or within inbred strains of mice, suggesting they are mediated through partially distinct mechanisms. In addition, these responses were assayed in the presence of several chloride channel inhibitors, including DIDS, diphenylamine-2-carboxylate, glibenclamide, and 5-nitro-2-(3-phenylpropylamino)-benzoic acid, and a protein kinase A inhibitor, the Rp diastereomer of adenosine 3′,5′-cyclic monophosphothioate ( Rp-cAMPS). The responses to low chloride and forskolin demonstrate significantly different pharmacological profiles to both DIDS and Rp-cAMPS, indicating that channels in addition to CFTR contribute to the low chloride response.

scholarly journals E1A-CR3 Interaction-Dependent and -Independent Functions of mSur2 in Viral Replication of Early Region 1A Mutants of Mouse Adenovirus Type 1

2005 ◽  
Vol 79 (6) ◽  
pp. 3267-3276 ◽  
Author(s):  
Lei Fang ◽  
Katherine R. Spindler
Keyword(s):  
Viral Replication ◽  
Adenovirus Type ◽  
Inbred Strains ◽  
Wild Type ◽  
Embryonic Fibroblasts ◽  
Early Region ◽  
Inbred Strains Of Mice ◽  
Independent Functions ◽  
A Subunit

ABSTRACT mSur2, a subunit of the Mediator complex, is required for efficient mouse adenovirus type 1 (MAV-1) replication (L. Fang, J. L. Stevens, A. J. Berk, and K. R. Spindler, J. Virol. 78:12888-12900, 2004). We examined the contributions of early-region 1A (E1A) to mSur2 function in MAV-1 replication with E1A mutant viruses. At a multiplicity of infection (MOI) of 1, viruses containing CR3 replicated better in Sur2+/+ mouse embryonic fibroblasts (MEFs) than in Sur2−/− MEFs. In contrast, viruses lacking CR3 replicated no better in Sur2+/+ than in Sur2−/− MEFs. This result supports the hypothesis that the E1A CR3-mSur2 interaction is important for MAV-1 replication. However, at an MOI of 0.05, viruses lacking CR3 showed replication defects in Sur2−/− MEFs compared to Sur2+/+ MEFs, suggesting an E1A CR3 interaction-independent function of mSur2 in MAV-1 replication in cell culture. Paradoxically, CR1Δ, CR2Δ, and CR3Δ mutant viruses replicated slightly more efficiently than wild-type (wt) MAV-1 and E1A null mutant viruses in Sur2−/− MEFs at an MOI of 0.05. Coinfection of Sur2−/− MEFs with wt MAV-1 and CR1Δ, CR2Δ, or CR3Δ mutant viruses rescued the defects of wt MAV-1 replication. This result suggests that an inhibiting effect on wt E1A protein expression and/or E1A function might account for the severe viral replication defect of MAV-1 in Sur2−/− MEFs at an MOI of 0.05. Moreover, titrations of virus yields from infected brains of inbred strains of mice showed that E1A null and CR3Δ mutant viruses had a significant defect in virus replication compared to wt MAV-1. This result supports the hypothesis that the MAV-1 E1A-mSur2 interaction is important in MAV-1 replication in mice.

scholarly journals Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain

2002 ◽  
Vol 83 (2) ◽  
pp. 351-358 ◽  
Author(s):  
Jaskamal Girn ◽  
Mojgan Kavoosi ◽  
Janet Chantler
Keyword(s):  
Viral Myocarditis ◽  
Neutralizing Antibody ◽  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Infected Cells ◽  
Group B ◽  
Multiple Strains ◽  
Old Mice

Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10–50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab′)2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1–2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual.

scholarly journals G Proteins Gαi1/3Are Critical Targets for Bordetella pertussis Toxin-Induced Vasoactive Amine Sensitization

2013 ◽  
Vol 82 (2) ◽  
pp. 773-782 ◽  
Author(s):  
Sean A. Diehl ◽  
Benjamin McElvany ◽  
Rajkumar Noubade ◽  
Nathan Seeberger ◽  
Brock Harding ◽  
...  
Keyword(s):  
Pertussis Toxin ◽  
Bordetella Pertussis ◽  
Inflammatory Responses ◽  
Whooping Cough ◽  
Differential Susceptibility ◽  
Inbred Strains ◽  
Content Type ◽  
Multiple Loci ◽  
Inbred Strains Of Mice

ABSTRACTPertussis toxin (PTX) is an AB5-type exotoxin produced by the bacteriumBordetella pertussis, the causative agent of whooping cough.In vivointoxication with PTX elicits a variety of immunologic and inflammatory responses, including vasoactive amine sensitization (VAAS) to histamine (HA), serotonin (5-HT), and bradykinin (BDK). Previously, by using a forward genetic approach, we identified the HA H1receptor (Hrh1/H1R) as the gene in mice that controls differential susceptibility toB. pertussisPTX-induced HA sensitization (Bphs). Here we show, by using inbred strains of mice, F1hybrids, and segregating populations, that, unlike Bphs, PTX-induced 5-HT sensitivity (Bpss) and BDK sensitivity (Bpbs) are recessive traits and are separately controlled by multiple loci unlinked to 5-HT and BDK receptors, respectively. Furthermore, we found that PTX sensitizes mice to HA independently of Toll-like receptor 4, a purported receptor for PTX, and that the VAAS properties of PTX are not dependent upon endothelial caveolae or endothelial nitric oxide synthase. Finally, by using mice deficient in individual Gαi/oG-protein subunits, we demonstrate that Gαi1and Gαi3are the criticalin vivotargets of ADP-ribosylation underlying VAAS elicited by PTX exposure.

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