Plasma Of Infected Mice Research Articles

Enhanced Platelet Adherence and Aggregation in Chagas' Disease: A Potential Pathogenic Mechanism for Cardiomyopathy

Spasm and thrombosis of the coronary microcirculation has been implicated in the pathogenesis of the cardiomyopathy of Chagas' disease. We demonstrate that increases in platelet adherence and aggregation accompany Trypanosoma cruzi infection and may contribute to the observed microvascular pathology. Scanning electron microscopy and radiolabeled platelets studies revealed that platelet adherence to T. cruzi-infected human endothelial cells was significantly increased when compared to controls (P = 0.024). In in vitro experiments, we determined the influence of infection on prostacyclin production, a marker of endothelial cell perturbation. The basal levels of 6-keto-prostaglandin F1 alpha was significantly greater in the supernatant of infected endothelial cells than in those of uninfected endothelial cells (P less than 0.05). The influence of infection was assessed on platelet aggregation at days 5 and 12 post-infection in A/J mice. Platelets from T. cruzi-infected mice were 2-6-fold more sensitive to aggregation induced by adenosine diphosphate and sodium arachidonate than controls. Thromboxane B2 levels in the plasma of infected mice were greater than controls. These data support the hypothesis that heightened platelet reactivity and endothelial cell dysfunction are associated with acute Chagas' disease and may cause coronary microvascular spasm and/or occlusion.

Evaluation of spleen lymphocyte responsiveness to a T-cell mitogen during early infection with larval Taenia taeniaeformis.

The effect of taeniid infection on the in vitro cellular response of the host was investigated. Infections of Taenia taeniaeformis decreased the ability of spleen cells from susceptible C3H/He mice to respond to the T-cell mitogen concanavalin A (Con A) as early as 2 days postinfection (pi) reaching a suppression peak at day 12 pi. Similar experiments performed with spleen cells from infected BALB/c mice, resistant to the infection, revealed little or no suppression of Con A stimulation. The results suggested that susceptibility to the parasite may be due to its ability to induce a partial suppression of the host's immune system. The role of adherent splenocytes from infected C3H/He mice in the production of a deficient response to Con A during early infection was studied by coculturing experiments. These experiments demonstrated that adherent populations from infected mice did not play a direct role in the Con A-suppressor mechanisms. Concomitant with the suppressor activity an increased background proliferation was observed with nonstimulated splenocytes from C3H/He mice infected with T. taeniaeformis. Plasma from infected mice was able to suppress the response of normal spleen cells to Con A and to stimulate a proliferative response in cultured splenocytes from noninfected animals. The results suggest the presence of factors in the plasma of infected mice which may be modulating the immune response to the parasite.

Age-Dependent Paralytic Viral Infection in C58 Mice: Possible Implications in Human Neurologic Disease

Publisher Summary This chapter analyzes the specific ways that aging, viral infection, genetic factors, and immune deficiency act together to predispose mice to paralytic disease using an age-dependent motor neuron disease in C58 mice as an experimental model. Lactic dehydrogenase virus (LDV) is widespread in both domestic and wild mice and causes life-long infection. Immune complexes typically are found in the plasma of infected mice. LDV does not cause significant pathologic changes in the tissues of infected mice under ordinary circumstances. The properties of LDV are summarized in the chapter. LDV derived from line Ib transplantable leukemia causes a fatal inflammatory motor neuron disease when inoculated into C58 mice that are 9 or more month of age, and in younger C58 mice, providing that they are immunosuppressed first by X-irradiation or drugs. LDV strains differ markedly in their neuropathogenicity ranging from those that are highly paralytic to those that cause inapparent infection.

Plasmodium berghei: Formation of secondary immune complexes in hyperimmune mice

BALB/c mice infected with the lethal malaria strain Plasmodium berghei (K 173) and hyperimmune BALB/c mice which had been recovered from the infection after chloroquine therapy were used to study the formation of immune complexes in glomeruli of the kidney and in plasma, and their role in the induction of nephropathies, using electron microscopy, immunofluorescence, immunoperoxidase, and immunodiffusion techniques. Electron microscopical studies revealed comparable ultrastructural alterations in the glomeruli of infected and hyperimmune mice. Immune complexes in the glomeruli of infected mice were found to consist of immunoglobulins IgM, IgA, and IgG, complement factor, and plasmodial antigens. On the other hand, precipitating plasmodial antibodies were hardly detectable in plasma of infected mice, while plasmodial antigens were present. An increased urinary protein content was recorded in infected mice. The sera were negative in the rheumatoid factor assay. Eradication of the parasitemia by chloroquine therapy caused a gradual disappearance of plasmodial antigens from the glomerular immune complexes and from plasma within 3 weeks. The glomeruli, however, remained strongly positive for immunoglobulins and complement. Plasma and glomeruli of hyperimmune mice which had been free of parasites up to 10 weeks remained strongly positive for immunoglobulins and complement and completely negative for plasmodial antigens. No increased urinary protein content was recorded. The sera were negative for rheumatoid factor. Intravenous injections of hyperimmune serum into normal control mice and into infected athymic nude mice caused in both cases a deposition of immune complexes in the glomeruli, being negative for plasmodial antigens in the control recipients and positive in the infected nude group. These findings provide evidence that P. berghei infection in BALB/c mice caused a nontransient deposition of immune complexes of two different types: a first type in which plasmodial antigens could be demonstrated during an acute infection and a second type in which plasmodial antigens could not be demonstrated and which occurred in the plasma of recovered hyperimmune mice.

Detection of endotoxins with the Limulus test in burned and unburned mice infected with different species of gram-negative bacteria.

The Limulus test detected endotoxins in the plasma of burned and unburned mice infected with different species of gram-negative bacteria produced different amounts of endotoxin in the plasma of infected mice. Plasma from mice given lethal infections showed very high concentrations of endotoxin. Low concentrations of endotoxin in the plasma were tolerated by mice but high concentrations were invariably fatal. A polyvalent pseudomonas vaccine reduced endotoxin in the plasma of mice given lethal infections of Pseudomonas aeruginosa.

Electron Microscopy of a Tumor Virus RNA

The structure of Friend leukemia virus (FLV) has been studied by electron microscopy. The virus was harvested from the plasma of infected mice and purified by techniques including differential velocity and isopycnic sucrose gradient centrifugation. Viral nucleic acid was isolated using GuHCl followed by precipitation with ethanol and resuspension in 1 mM dithiothreitol. In initial experiments, the RNA solution was diluted 1:10 into either H2O or 4-8 M urea. Prior to spreading, 1 M ammonium acetate and cytochrome c were added to a final concentration of 0.4 M and 0.01% respectively. Fifty μ1 of this mixture was spread using a glass slide inclined in a ten cm2 trough filled with 15 mM ammonium acetate. Samples were picked up on collodion filmed grids, stained with uranyl acetate and rotary shadowed with Pt:Pd. This method is very similar to the conditions used to study the RNA of avian myeloblastosis virus, murine leukemia virus, and mammary tumor virus (MTV).

Studies on the mechanism of action of Riley virus. IV. The reticuloendothelial system and impaired plasma enzyme clearance in infected mice.

The plasma clearance of intravenously injected rabbit muscle LDH was studied. In normal mice the clearance followed a biphasic exponential curve comprising an initial fast and subsequent slow phase. Riley virus-infected mice showed only the slow phase of enzyme clearance. The change from fast to slow clearance rate in normal mice appeared to depend upon the level of plasma enzyme activity rather than on the amount of enzyme cleared. Treatment of mice with RES-blocking agents (cholesterol oleate and carbon) inhibited the fast clearance phase, whereas an RES-stimulating agent (stilbestrol) caused an accelerated rate of enzyme clearance. Riley virus infection was found to inhibit the clearance of phosphoglucose isomerase, but had no effect on the clearance of alanine transaminase. The activity of the former enzyme is raised in the plasma of infected mice, whereas the activity of the latter enzyme is unaltered.

Riley virus neutralizing activity in the plasma of infected mice with persistent viraemia

Lactate dehydrogenase-elevating virus (LDV) is a mouse arterivirus, unusual in its extreme host specificity and its persistence in the circulation of the infected host that naturally infects wild mice. Although, probably not as frequent in laboratory mouse colonies as it used to be, LDV infection may affect experimental results, primarily through its effects on the host immune responses. On the other hand, because of its unique properties, LDV infections serve as a good animal model for viral persistence, virally induced immunomodulation, and pathogenic infection of neurons in the central nervous system. However, the inability of LDV to infect in transformed cell lines and to cause a detectable cytopathic effect in cell cultures in which it replicates, such as mouse peritoneal exudate cells, represents technical obstacles to the further analysis of this virus. Identification of the cell receptor utilized by LDV would constitute a major advance, since this might lead to the creation of a cell line permissive to LDV infection. Whereas LDV is a natural and sometimes pathogenic infectious agent of the mouse, it does not currently represent a major threat to animal facilities. The virus is not very contagious and there are a number of easy methods available to detect infected mice. Moreover, further study of the interaction between relatively silent viruses, such as LDV, and their host species should lead to new insights into the mechanisms by which viruses can establish and maintain relatively harmless, persistent infections in their hosts.

ISOENZYMIC SPECIFICITY OF IMPAIRED CLEARANCE IN MICE INFECTED WITH RILEY VIRUS.

The clearance from the plasma of purified lactate dehydrogenase isoenzyme No. 5, which is increased in the plasma of mice infected with Riley virus, is impaired during the infection. That the clearance of purified isoenzyme No. 1 is unchanged by infection with Riley virus provides an explanation of why only the lactate dehydrogenase-5 isoenzyme activity is elevated in the plasma of infected mice.