Microbiology and Immunology

1980

DOI: 10.1111/j.1348-0421.1980.tb00584.x

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Enhanced Phagocytic Activity of Macrophages in Mouse Hepatitis Virus‐Infected Nude Mice

¹

,

Akiko Sakaguchi

²

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³

et al.

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Chronic Infections2

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1982

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Cited by 12 publications

(5 citation statements)

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“…Although many viral infections result in a decrease in macrophage functions, including phagocytosis, some viruses, such as herpes simplex virus (2), Coxsackie virus (22), or Newcastle disease virus (19), have been shown to enhance the ability of these cells to incorporate various targets. Whereas contradictory results have been reported after LDV infection (17,18,32), another nidovirus, mouse hepatitis virus, can also increase macrophage-mediated phagocytosis (33).…”

Section: Discussionmentioning

confidence: 90%

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

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²

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³

et al. 2000

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Strong enhancement of the pathogenicity of an antierythrocyte monoclonal antibody was observed after infection of mice with lactate dehydrogenase-elevating virus. While injection of the antierythrocyte antibody alone induced only moderate anemia, concomitant infection with this virus, which is harmless in most normal mice, led to a dramatic drop in the hematocrit and to death of infected animals. In vitro and in vivo analyses showed a dramatic increase in the ability of macrophages from infected mice to phagocytose antibody-coated erythrocytes. These results indicate that viruses can trigger the onset of autoimmune disease by enhancing the pathogenicity of autoantibodies. They may explain how unrelated viruses could be implicated in the etiology of autoantibody-mediated autoimmune diseases.A causal connection between viral infection and the development of clinical pathology has long been suspected for a number of autoimmune diseases mediated by autoantibodies (reviewed in reference 36). Interestingly, in most cases, several different viruses have been proposed as etiologic agents of the same disease. Experimental data have suggested that viruses trigger an autoimmune humoral response by distinct mechanisms, including polyclonal B-lymphocyte activation, antigenic mimicry, modification of self-antigen, production of anti-idiotypic antibodies, or enhancement of major histocompatibility complex molecule expression on potential antigen-presenting cells (4,9,11,15,20,25,31,37). However, although it has been conclusively shown in several models that autoantibody secretion was triggered by infection, the actual pathogenicity of these antibodies has not always been demonstrated. Similarly, other stimuli, like immunization of mice with rat red blood cells, may lead to autoantibody production without development of the corresponding disease, in this case, hemolytic anemia (8,24,34). Therefore, it may be that mere autoantibody secretion is not sufficient to trigger an autoimmune disease and that the immune environment of the host plays an important role in the pathogenicity of such autoantibodies.Viruses have also been shown to variably affect macrophage functions, including cytokine production and the ability to present antigens (6, 16). Since it is known that some autoantibody-mediated diseases involve phagocytosis by macrophages, we postulated that modulation of this cellular function may explain the induction of such clinical diseases observed in the course of viral infections. To test this hypothesis, we used an experimental model of anemia induced by administration of antierythrocyte monoclonal antibodies (29). Our results indicate that a viral infection with lactate dehydrogenase-elevating virus (LDV) may trigger a dramatic hemolytic disease by enhancing the pathogenicity of autoantibodies. If confirmed with other models, this observation may indicate how different viruses can trigger similar clinical autoimmune diseases and open the way to novel therapeutic approaches. MATERIALS AND METHODSMice. Female BALB/c mice w...

“…Although many viral infections result in a decrease in macrophage functions, including phagocytosis, some viruses, such as herpes simplex virus (2), Coxsackie virus (22), or Newcastle disease virus (19), have been shown to enhance the ability of these cells to incorporate various targets. Whereas contradictory results have been reported after LDV infection (17,18,32), another nidovirus, mouse hepatitis virus, can also increase macrophage-mediated phagocytosis (33).…”

Section: Discussionmentioning

confidence: 90%

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

¹

,

²

,

³

et al. 2000

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Strong enhancement of the pathogenicity of an antierythrocyte monoclonal antibody was observed after infection of mice with lactate dehydrogenase-elevating virus. While injection of the antierythrocyte antibody alone induced only moderate anemia, concomitant infection with this virus, which is harmless in most normal mice, led to a dramatic drop in the hematocrit and to death of infected animals. In vitro and in vivo analyses showed a dramatic increase in the ability of macrophages from infected mice to phagocytose antibody-coated erythrocytes. These results indicate that viruses can trigger the onset of autoimmune disease by enhancing the pathogenicity of autoantibodies. They may explain how unrelated viruses could be implicated in the etiology of autoantibody-mediated autoimmune diseases.A causal connection between viral infection and the development of clinical pathology has long been suspected for a number of autoimmune diseases mediated by autoantibodies (reviewed in reference 36). Interestingly, in most cases, several different viruses have been proposed as etiologic agents of the same disease. Experimental data have suggested that viruses trigger an autoimmune humoral response by distinct mechanisms, including polyclonal B-lymphocyte activation, antigenic mimicry, modification of self-antigen, production of anti-idiotypic antibodies, or enhancement of major histocompatibility complex molecule expression on potential antigen-presenting cells (4,9,11,15,20,25,31,37). However, although it has been conclusively shown in several models that autoantibody secretion was triggered by infection, the actual pathogenicity of these antibodies has not always been demonstrated. Similarly, other stimuli, like immunization of mice with rat red blood cells, may lead to autoantibody production without development of the corresponding disease, in this case, hemolytic anemia (8,24,34). Therefore, it may be that mere autoantibody secretion is not sufficient to trigger an autoimmune disease and that the immune environment of the host plays an important role in the pathogenicity of such autoantibodies.Viruses have also been shown to variably affect macrophage functions, including cytokine production and the ability to present antigens (6, 16). Since it is known that some autoantibody-mediated diseases involve phagocytosis by macrophages, we postulated that modulation of this cellular function may explain the induction of such clinical diseases observed in the course of viral infections. To test this hypothesis, we used an experimental model of anemia induced by administration of antierythrocyte monoclonal antibodies (29). Our results indicate that a viral infection with lactate dehydrogenase-elevating virus (LDV) may trigger a dramatic hemolytic disease by enhancing the pathogenicity of autoantibodies. If confirmed with other models, this observation may indicate how different viruses can trigger similar clinical autoimmune diseases and open the way to novel therapeutic approaches. MATERIALS AND METHODSMice. Female BALB/c mice w...

“…It is not pathogenic for heterozygote nul + mice with a Balbi c background. Interestingly, Tamura et al (1977Tamura et al ( , 1978Tamura et al ( , 1980 found in infected athymic nulnu mice an immune response normally not detectable in these animals. After inoculation with thymus-dependent antigen (sheep red blood cells), chronically infected nulnu mice produce neutralizing antibodies (lgM and IgG) and also produce a secondary response .…”

Section: Chronic Infectionsmentioning

confidence: 93%

“…Additionally, during the early phase of disease; the phagocytic activity and number of macrophages is enhanced. Impairment of macrophage functions by the toxic effects of silica inoculation aggravates the disease course and leads to a lethal acute hepatitis (Tamura et al , 1980.…”

Section: Chronic Infectionsmentioning

confidence: 99%

The Biology and Pathogenesis of Coronaviruses

Wege¹,

1982

Current Topics in Microbiology and Immunology

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No abstract

“…MHV has served as a model for the molecular biology of coronaviruses, viral hepatitis, encepha~ litis and demyelination, as well as a model for genetic and age-related resistance to viral disease (2,21,23,25,31). MHV can cause significant clinical disease in mice (4) or a number of more subtle but equally significant effects, including modified immune responsiveness (27,36), an effect upon tumor kinetics (1,7,12,20,22) and effects upon macrophage function (6,34) which can negate the research usefulness of the infected animal.…”

Section: Introductionmentioning

confidence: 99%

Mouse hepatitis virus strain — Related patterns of tissue tropism in suckling mice

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²

1984

Archives of Virology

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The pattern of tissue tropism for several prototype and uncharacterized strains of mouse hepatitis virus (MHV) was studied by intranasal inoculation of each virus strain into groups of neonatal Swiss mice under otherwise identical conditions. Mice were killed at intervals up to 18 days after inoculation, and their tissues were examined for the presence of MHV antigen by indirect immunofluorescence. Two patterns of infection were apparent. Prototype MHV strains 1, 3, A59, JHM, S and uncharacterized MHV strains Tettnang and wt-1 produced a respiratory pattern, in which nose and lung were consistently involved with dissemination to other organs in a vascular distribution. Pulmonary vascular endothelium and alveolar septal cells, but not airway epithelium, were infected. An enteric pattern was observed with MHV-Y and wt-2 in which MHV antigen was largely restricted to the nose and bowel, with limited dissemination to other abdominal organs but not lung. Intestinal lesions in these mice were severe compared to those manifesting the respiratory pattern of infection. These results indicate that, like coronaviruses of other species, different strains of MHV possess different primary and secondary organotropisms following a natural route of inoculation in a susceptible host.

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