Effect of silica on virus infections in mice and mouse tissue culture

duBuy, H. G.

doi:10.1128/iai.11.5.996-1002.1975

Cited by 37 publications

(12 citation statements)

References 8 publications

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“…Silica has been used as a selective macrophage-toxic agent since the early 1960s in many animal experiments to evaluate the role of macrophages in the host response to virus infections. With most viruses examined, silica has been found to potentiate the invasion and spread of the infection to target organs (3,7,(12)(13)(14)(15)(16). In a few instances, silica treatment has, however, failed to break down resistance to infection (4) or has even enhanced the resistance (5).…”

Section: Discussionmentioning

confidence: 99%

Effect of silica on the pathogenic distinction between herpes simplex virus type 1 and 2 hepatitis in mice

Mogensen¹,

Andersen²

1977

Infect Immun

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The role of macrophages in the difference in liver pathogenicity between herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) in mice was investigated by selectively blocking the macrophage function of the mice by silica. Intravenous administration of 3 mg of silica 2 h before virus inoculation partially abolished the difference between the two virus types, as judged by macroscopic and microscopic examination of the livers and by virus isolation studies. Intraperitoneal inoculation of 50 mg of silica before virus seemed more effective in suppressing the macrophage function, since this treatment almost completely eliminated the difference in hepatotropism between HSV-1 and HSV-2 as assessed by the number and size of the lesions appearing in the liver. The final outcome of the infection, death from encephalitis, was, however, not influenced by macrophage blockade.In a previous study it was shown that a specific pathogenic distinction exists between herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infection in mice (11). On intraperitoneal (i.p.) inoculation with strains of HSV-2, most mice develop progressive focal necrotizing hepatitis, whereas HSV-1 only occasionally produces a few tiny self-limiting foci of necrosis in the liver.Recently, the role of macrophages in this difference in pathogenicity between the two closely related virus types was examined, and results were presented which indicated that macrophages might play a crucial part in the phenomenon, as it was shown that the restriction of HSV-1 replication in peritoneal macrophages from mice was much greater than that of HSV-2 replication (10).Silica, an agent reported to be selectively toxic for macrophages (2, 6), has been used in several studies to delineate the role of macrophages in the host defense mechanisms against a variety of virus infections (3-5, 7, 12-16). The purpose of the present study was to add further evidence to the role of macrophages in the pathogenic action of HSV-1 and HSV-2 in mice by selectively blocking the macrophage cell population by administration of silica.MATERIALS AND METHODS Mice. Four-week-old female inbred specific-path ogen-free mice of the BALB/c/A/BOM strain were used. They were obtained from Gl. Bomholtgaard Viruses. HSV strains MacIntyre (HSV-1) and MS (HSV-2), used in this study, were described previously (11). Silica. Silica in the form of Dorentrup Quartz no. 12 (<5 gm) was kindly provided by and has been found active for macrophage blockade in his hands (J. Lindenmann, personal communication). Dry, autoclaved silica was suspended in phosphate-buffered saline just before use at a concentration of 15 mg/ml for intravenous (i.v.) and 50 mg/ml for i.p. injection. Immediately before injection it was dispersed by brief exposure to ultrasonic vibration.In vivo experiments. Silica was injected slowly in the tail vein (3 mg/0.2 ml) of 4-week-old BALB/c mice. Two hours after the silica injection, the mice were inoculated i.p. with 105 plaque-forming units of either HSV-1 or HSV-2 in 0.1 ml of diluent. Groups...

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Section: Discussionmentioning

confidence: 99%

Effect of silica on the pathogenic distinction between herpes simplex virus type 1 and 2 hepatitis in mice

Mogensen¹,

Andersen²

1977

Infect Immun

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“…Treatment of mice with certain regimens of silica can actually increase phagocytic activity in the mouse (duBuy, 1975 ;McCord and Morahan, unpublished observations).…”

Section: Discussionmentioning

confidence: 94%

Macrophage activation and anti‐tumor activity of biologic and synthetic agents

Morahan

Kaplan

1976

Intl Journal of Cancer

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Systemic administration of the synthetic immunopotentiator pyran, was as effective as the use of the biologic immunopotentiator BCG in activating macrophages and in inhibiting the Lewis lung carcinoma and MCA 2182 sarcoma. Several other synthetic polyanions also activated macrophages and exhibited some anti-tumor activity, but none were as effective as pyran. Cell-wall fractions such as the Ribi vaccine and MER were considerably less effective than BCG. The anti-tumor activity of pyran against the virtually non-immunogenic Lewis lung carcinoma involved non-specifically activated macrophages, and both anti-tumor activity and macrophage activating ability persisted over a 100-fold range of drug from 0.5 mg/kg to 50 mg/kg. The ability of activated macrophages to destroy tumor cells was abrogated by treatment with trypan blue, an inhibitor of macrophage lysosomal enzymes. In addition, preincubation of tumor cells with activated peritoneal cells at effector-cell:target-cell ratios of 20:1 and 5:1 markedly decreased tumor incidence and mortality. Glycogen-stimulated or unstimulated peritoneal cells were completely inactive in inhibiting tumor growth in vivo or exhibiting cytotoxicity in vitro, demonstrating the requirement for activated macrophages selective for tumor-cell destruction.

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“…In contrast to the effect obtained in vitro (1), in vivo injection (i.p.) first results in a destruction of resident macrophages followed by a rebound of immature macrophages from the bone marrow (10). Silica treatment of mice increased virus content of the visceral organs and mortality after HSV infection (8,44).…”

Section: Developmentmentioning

confidence: 99%

Kinetics and genetics of herpes simplex virus-induced antibody formation in mice

Knoblich¹,

Görtz²,

Harle-Grupp³

et al. 1983

Infect Immun

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The kinetics of antibody synthesis was investigated after intraperitoneal, subcutaneous, and footpad infection of various strains of mice with herpes simplex virus. Immunoglobulin M antibodies appeared 5 days after and immunoglobulin G antibodies appeared 10 to 12 days after intraperitoneal infection with herpes simplex virus type 1. The major histocompatibility complex and the background genome of inbred mice were not found to have a systematical influence on antibody synthesis. Female mice, however, consistently produced more antibodies than did male if the infection was done intraperitoneally, but not if it was done subcutaneously or into footpads. Castration considerably increased the amount of antibodies produced by male mice. The difference in antibody formation between females and males could be abolished by injection of silica; moreover, antibody titers were enhanced by this treatment. This has also been found by immunization with a Formalin-inactivated herpes simplex virus vaccine. The effect of silica in enhancing antibody formation could be observed up to 12 days after infection. Infectious virus could be detected up to 2 days after infection, and herpes simplex virus type 1 antibody-stimulating antigens could be detected up to 4 days in ultrasonicates of macrophages. The assumption is made that androgen-sensitive cell populations, including macrophages and their soluble products, are involved in antibody-depressing mechanisms.

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Effect of silica on virus infections in mice and mouse tissue culture

Cited by 37 publications

References 8 publications

Effect of silica on the pathogenic distinction between herpes simplex virus type 1 and 2 hepatitis in mice

Effect of silica on the pathogenic distinction between herpes simplex virus type 1 and 2 hepatitis in mice

Macrophage activation and anti‐tumor activity of biologic and synthetic agents

Kinetics and genetics of herpes simplex virus-induced antibody formation in mice

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