Coxsackie B1 virus infection enhances the bacterial invasiveness, the phagocytosis and the membrane permeability in HEp‐2 cells

Modalsli, Kristin; Bukholm, Geir; Degré, Miklos

doi:10.1111/j.1699-0463.1990.tb01061.x

Cited by 9 publications

(21 citation statements)

References 8 publications

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“…5). 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: 99%

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

Meité

Léonard

Idrissi

et al. 2000

J Virol

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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...

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Section: Discussionmentioning

confidence: 99%

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

Meité

Léonard

Idrissi

et al. 2000

J Virol

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“…Moreover, it has also been observed that coinfections of HEp-2 cells with enteroviruses and Campylobacter isolates resulted in an increase of bacterial invasion (Konkel and Joens 1990). Coxsackievirus B 1 has also been reported to induce an enhancement of invasion of Shigella flexneri in HEp-2 cells, which correlated with an increase of induced phagocytosis (Modalsli et al 1990). Recently, we observed an increase in invasion ability of S. flexneri in different cell lines infected with poliovirus or other enteroviruses (Marchetti et al 1992;Seganti et al 1994).…”

Section: Introductionmentioning

confidence: 98%

Superinfection by Listeria monocytogenes of cultured human enterocyte-like cells infected with poliovirus or rotavirus

Superti

Petrone

Pisani

et al. 1996

Medical Microbiology and Immunology

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A mixed infection with either rotavirus or poliovirus and Listeria monocytogenes was analysed in Caco-2 cells, a tumour-derived cell line, highly susceptible to these pathogens. The multiplication of these pathogens, whose usual site of entry and/or replication is the intestine, was also followed by electron microscopy. Results obtained showed an increase of L. monocytogenes internalisation in cells infected with rotavirus, whereas the preinfection with poliovirus had only a slight interfering effect on bacterial entry. Analysis of L. monocytogenes multiplication in virus-infected cells revealed that rotavirus also promoted bacterial replication, which poliovirus hampered replication. Concerning the effect of Caco-2 cell invasion by L. monocytogenes on viral replication, we observed an increase in rotavirus antigen synthesis but no significant effect on poliovirus yield under our experimental conditions.

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“…This enhancement can be divided into two phases: an early and a late phase. The early phase enhancement, up to 3 h after inoculation, can be reproduced by pretreating cells with UVinactivated virus (12) and is not dependent on protein synthesis (15). In contrast, the late phase effect, 6 h after virus inoculation, requires viable virus (12) and coincides with protein synthesis (15).…”

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confidence: 97%

“…Cellular alterations induced by viral infections have a significant effect on the ability of bacteria to adhere to and invade cells. Several investigators have demonstrated that virus infection results in an increase in bacterial adherence (6,7,16) and invasiveness (7,12). Infection of HEp-2 cell cultures with coxsackie B1 virus enhanced the invasiveness of Shigella flexneri (12).…”

mentioning

confidence: 99%

“…The early phase enhancement, up to 3 h after inoculation, can be reproduced by pretreating cells with UVinactivated virus (12) and is not dependent on protein synthesis (15). In contrast, the late phase effect, 6 h after virus inoculation, requires viable virus (12) and coincides with protein synthesis (15). Several other cellular functions such as plasma membrane permeability (12), non-receptor-mediated phagocytosis (6), and Na+-K+-activated ATPase activity (14) are altered in the early phase of the virus infection cycle.…”

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confidence: 99%

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Microinjection of HEp-2 cells with coxsackie B1 virus RNA enhances invasiveness of Shigella flexneri only after prestimulation with UV-inactivated virus

Modalsli¹,

Mikalsen²,

Bukholm³

et al. 1993

Apmis

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Coxsackie B1 virus induces increased susceptibility to invasion by Shigella flexneri when HEp‐2 cells are inoculated with the complete virus. When RNA from the same virus was microinjected into cells, virus RNA was synthesized and new virus particles were formed, but the transfected RNA had no effect on bacterial invasiveness. However, when the cells were prestimulated with UV‐inactivated virus, the microinjected RNA induced an additional enhancement of bacterial invasiveness. Microinjected whole virus particles did not replicate and did not induce any change in bacterial invasiveness. The results indicate that an initial event in virus multiplication is necessary to achieve an effect of transfected viral RNA on invasion of S. flexneri.

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Coxsackie B1 virus infection enhances the bacterial invasiveness, the phagocytosis and the membrane permeability in HEp‐2 cells

Cited by 9 publications

References 8 publications

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

Superinfection by Listeria monocytogenes of cultured human enterocyte-like cells infected with poliovirus or rotavirus

Microinjection of HEp-2 cells with coxsackie B1 virus RNA enhances invasiveness of Shigella flexneri only after prestimulation with UV-inactivated virus

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