scholarly journals Human platelet antigen (HPA)-1a peptides do not reliably suppress anti-HPA-1a responses using a humanized severe combined immunodeficiency (SCID) mouse model

2014 ◽  
Vol 176 (1) ◽  
pp. 23-36 ◽  
Author(s):  
D. J. Jackson ◽  
J. L. Eastlake ◽  
B. M. Kumpel
Keyword(s):  
Mouse Model ◽  
Scid Mouse ◽  
Human Platelet ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
Platelet Antigen ◽  
Human Platelet Antigen ◽  
Scid Mouse Model

scholarly journals The therapeutic use of osmotic minipumps in the severe combined immunodeficiency (SCID) mouse model for rheumatoid arthritis

2008 ◽  
Vol 68 (1) ◽  
pp. 124-129 ◽  
Author(s):  
A Knedla ◽  
B Riepl ◽  
S Lefèvre ◽  
S Kistella ◽  
J Grifka ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mouse Model ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Protective Effects ◽  
Combined Immunodeficiency ◽  
Human Cartilage ◽  
Osmotic Minipumps ◽  
Osmotic Pumps ◽  
Scid Mouse Model

Objectives:The viral gene transfer of interleukin 1 receptor antagonist (IL1ra) and interleukin 10 (IL10) into rheumatoid arthritis (RA) synovial fibroblasts (RASFs) has shown protective effects on cartilage destruction in the severe combined immunodeficiency (SCID) mouse model of RA. Nevertheless, side effects of viral transduction are possible and a number of cytokines or cytokine inhibitors are not available encoded in viral vehicles. As the production of viruses coding for bioactive proteins is cost and time intensive, we established an in vivo long-term release model using osmotic minipumps in the SCID mouse model for RA.Methods:Isolated RASFs were cultured for four passages and coimplanted together with human cartilage and an Alzet osmotic miniature pump model 2004, containing 200 μl of IL10 and IL1ra for 40 days in SCID mice. Implants were removed after 40 days and evaluated histologically. The actual rates of IL10 and IL1ra in murine serum were measured by ELISA.Results:Release of IL10 and IL1ra by the pumps was effective as both could be measured in significant amounts in the serum of the mice. IL10 and IL1ra release showed protective effects towards the coimplanted cartilage, similar to the adenovirally IL10/IL1ra-transduced RASFs. The mean (SD) invasion scores for the implants with the osmotic pumps were: invasion 0.7 (0.5), degradation 0.5 (0.3) (all parameters significant vs controls, p<0.05).Conclusions:The results demonstrate that the combination of osmotic pumps with the SCID mouse model for RA can be used as approach for application and evaluation of cartilage-protective molecules. Furthermore, the effect of cartilage-protective cytokines is independent of the type of application.

Assessment of human platelet survival in the NOD/SCID mouse model: technical considerations

Transfusion ◽  
2016 ◽  
Vol 56 (6) ◽  
pp. 1370-1376 ◽  
Author(s):  
Julia Fuhrmann ◽  
Rabie Jouni ◽  
Jenny Alex ◽  
Heike Zöllner ◽  
Jan Wesche ◽  
...  
Keyword(s):  
Mouse Model ◽  
Scid Mouse ◽  
Human Platelet ◽  
Platelet Survival ◽  
Scid Mouse Model ◽  
Technical Considerations

scholarly journals P38 mitogen activated protein kinase inhibitor improves platelet in vitro parameters and in vivo survival in a SCID mouse model of transfusion for platelets stored at cold or temperature cycled conditions for 14 days

PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0250120
Author(s):  
Andrey Skripchenko ◽  
Monique P. Gelderman ◽  
Jaroslav G. Vostal
Keyword(s):  
Mouse Model ◽  
Cold Storage ◽  
Scid Mouse ◽  
Room Temperature ◽  
Human Platelet ◽  
Human Platelets ◽  
Bacterial Proliferation ◽  
Scid Mouse Model

Platelets for transfusion are stored at room temperature (20–24°C) up to 7 days but decline in biochemical and morphological parameters during storage and can support bacterial proliferation. This decline is reduced with p38MAPK inhibitor, VX-702. Storage of platelets in the cold (4–6°C) can reduce bacterial proliferation but platelets get activated and have reduced circulation when transfused. Thermocycling (cold storage with brief periodic warm ups) reduces some of the effects of cold storage. We evaluated in vitro properties and in vivo circulation in SCID mouse model of human platelet transfusion of platelets stored in cold or thermocycled for 14 days with and without VX-702. Apheresis platelet units (N = 15) were each aliquoted into five storage bags and stored under different conditions: room temperature; cold temperature; thermocycled temperature; cold temperature with VX-702; thermocycled temperature with VX-702. Platelet in vitro parameters were evaluated at 1, 7 and 14 days. On day 14, platelets were infused into SCID mice to assess their retention in circulation by flow cytometry. VX-702 reduced negative platelet parameters associated with cold and thermocycled storage such as an increase in expression of activation markers CD62, CD63 and of phosphatidylserine (marker of apoptosis measured by Annexin binding) and lowered the rise in lactate (marker of increase in anaerobic metabolism). However, VX-702 did not inhibit agonist-induced platelet aggregation indicating that it does not interfere with platelet hemostatic function. In vivo, VX-702 improved initial recovery and area under the curve in circulation of human platelets infused into a mouse model that has been previously validated against a human platelet infusion clinical trial. In conclusion, inhibition of p38MAPK during 14-days platelet storage in cold or thermocycling conditions improved in vitro platelet parameters and platelet circulation in the mouse model indicating that VX-702 may improve cell physiology and clinical performance of human platelets stored in cold conditions.

scholarly journals A NOD/SCID mouse model for the assessment of human platelet aggregation in vivo

2012 ◽  
Vol 10 (3) ◽  
pp. 490-492 ◽  
Author(s):  
L. HOLBROOK ◽  
C. MOORE ◽  
D. SANZ-ROSA ◽  
A. SOLOMON ◽  
M. EMERSON
Keyword(s):  
Platelet Aggregation ◽  
Mouse Model ◽  
Scid Mouse ◽  
Human Platelet ◽  
Human Platelet Aggregation ◽  
Scid Mouse Model

Propagation of Human Papillomavirus Type 11 in Human Xenografts Using the Severe Combined Immunodeficiency (SCID) Mouse and Comparison to the Nude Mouse Model

Virology ◽  
1993 ◽  
Vol 197 (1) ◽  
pp. 455-458 ◽  
Author(s):  
William Bonnez ◽  
Robert C. Rose ◽  
Carrie Da Rin ◽  
Christine Borkhuis ◽  
Karen L. de Mesy Jensen ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Mouse Model ◽  
Nude Mouse ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
Nude Mouse Model

scholarly journals In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria.

1995 ◽  
Vol 182 (3) ◽  
pp. 643-653 ◽  
Author(s):  
K Willimann ◽  
H Matile ◽  
N A Weiss ◽  
B A Imhof
Keyword(s):  
Plasmodium Falciparum ◽  
Mouse Model ◽  
Cerebral Malaria ◽  
Mouse Brain ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Human Erythrocytes ◽  
Combined Immunodeficiency ◽  
The Brain

Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.

scholarly journals The Pathogenesis of HIV-Associated Dementia: Recent Advances Using a SCID Mouse Model of HIV-Encephalitis

2016 ◽  
Vol 22 (1) ◽  
pp. 32 ◽  
Author(s):  
Jennifer Cook ◽  
William Tyor
Keyword(s):  
Mouse Model ◽  
Highly Active Antiretroviral Therapy ◽  
Scid Mouse ◽  
Animal Studies ◽  
Severe Combined Immunodeficiency ◽  
Clinical Information ◽  
Neurological Complications ◽  
Future Research ◽  
Hiv Encephalitis ◽  
Scid Mouse Model

In the era of highly active antiretroviral therapy (HAART) there has been a decrease in AIDS death rates and a reduction in HIV-related neurological complications. However, Human Immunodeficiency Virus-1 (HIV)-associated dementia (HAD) still affects at least 7% of HIV-positive individuals. Despite significant advances in HIV research there are still questions surrounding the pathogenesis of HAD. Clinical information and pathological studies suggest that the frontal cortex, basal ganglia, and hippocampus are important neuroanatomical areas involved in HAD. Recent studies utilizing a severe combined immunodeficiency (SCID) mouse model of HIV-encephalitis (HIVE) indicate that central nervous system (CNS) viral load determines the severity of astrogliosis, an important feature of HIVE. Human and animal studies suggest that viral strains may also be important in the pathogenesis of HAD. A recent study suggests that HAART does not eradicate virus in the brain, and therefore, the CNS is a reservoir for HIV. Future research efforts need to focus on the role of viral strain and mutations in the pathogenesis of HAD. 

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