Mechanism of Protection During the Early Phase of a Generalized Viral Infection. I. Contribution of Phagocytes to Protection against Ectromelia Virus

Tsuru, Sumiaki; Kitani, Hideo; Seno, Masao; Abe, Mitsunobu; Zinnaka, Yutaka; Nomoto, Kikuo

doi:10.1099/0022-1317-64-9-2021

Cited by 23 publications

(20 citation statements)

References 15 publications

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“…It has already been shown that the pretreatment of suckling mice with syngeneic adult macrophages before MCMV infection resulted in a significant decrease of the percent mortality compared with mice without cell transfer, and that pretreatment of mice with silica before MCMV infection resulted in greater mortality as compared to control mice (31). Macrophages can be depleted by the administration of silica (12,25,31), asbestos (12), carrageenan (32,38), and by a number of other treatments (34,38). However, none of these treatments results in the complete depletion of all macrophage subpopulations.…”

Section: Discussionmentioning

confidence: 99%

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Hamano

Yoshida

Takimoto

et al. 1998

Microbiology and Immunology

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It has been recognized that macrophages play an important role in controlling virus infection in experimental animal models. To evaluate the role of macrophages in acute murine cytomegalovirus infection, macrophages in the spleen and the liver were eliminated by an intravenous injection of liposomes containing a cytolytic agent, dichloromethylene diphosphonate. The depletion of macrophages led to a significant increase of virus titer in the spleen and lungs in both susceptible BALB/c and resistant C57BL/6 mice during the first three days after intravenous infection. In the spleen, the increase of virus titer in macrophagedepleted BALB/c mice was much greater than that in NK cell-depleted mice. These results suggest that macrophages contribute to protection mainly by the mechanisms which are independent of NK cells during the first three days after infection. The increase of virus titer in macrophage-depleted C57BL/6 mice was as great as that in NK cell-depleted mice because of the high contribution of NK cells to protection in C57BL/6 mice. In the liver in both strains of mice, the effects of macrophage depletion on virus titer were not as much as those in the spleen and lungs. Furthermore, the local depletion of peritoneal macrophages resulted in a great increase of virus titer in the spleen at three days after intraperitoneal infection. We conclude that macrophages greatly contribute to decreasing the virus load in some organs possibly through either or both intrinsic and extrinsic mechanisms in the early phase of primary infection with murine cytomegalovirus.

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Section: Discussionmentioning

confidence: 99%

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Hamano

Yoshida

Takimoto

et al. 1998

Microbiology and Immunology

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“…Carrageenan type II (Sigma) was dissolved in distilled water (10 mg/ml). Mice were injected intraperitoneally with carrageenan (200 mg/kg) to deplete mainly tissue macrophages in the liver and spleen, and blood monocytes (Catanzaro et at., 1971) as well as to increase PMN in the blood (Tatsukawa et al, 1979;Tsuru et al, 1983). To impair the function of alveolar macrophages, 50 gl of carrageenan (1 mg/ml) diluted in MEM was administered intranasally to mice (2 mg/kg) 2 days before the virus infection.…”

Section: Methodsmentioning

confidence: 99%

“…In contrast, little is known of the protective role of such phagocytes in the early phase of generalized virus infection prior to the development of specific immune responses. In a previous study, we noted a significant role of macrophages in early protection against ectromelia virus infection in mice (Tsuru et al, 1983). However, there has been little study of the potential contribution of PMN to protection in the early phase against virus infections in vivo.…”

Section: Introductionmentioning

confidence: 99%

Protective Mechanisms against Pulmonary Infection with Influenza Virus. I. Relative Contribution of Polymorphonuclear Leukocytes and of Alveolar Macrophages to Protection during the Early Phase of Intranasal Infection

Fujisawa

Tsuru

Taniguchi

et al. 1987

Journal of General Virology

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SUMMARYThe relative contribution of polymorphonuclear leukocytes and macrophages in the early protection against intranasal infection of mice with influenza virus was investigated. Virus multiplication in the lung in the early phase of infection with less than 1.5 x 10 3 plaque-forming units was enhanced by X-ray irradiation. The intranasal administration of carrageenan did not influence the titre of virus. However, when mice were infected with 1.5 x 10 4 plaque-forming units, the virus titre was elevated by intranasal administration of carrageenan as well as by X-ray irradiation, but not by intraperitoneal administration of carrageenan. The intranasal administration of carrageenan not only inhibited the phagocytic activity of alveolar macrophages but also enhanced susceptibility to the virus. On the other hand, polymorphonuclear leukocytes were capable of phagocytosing the virus in vitro and were non-permissive for virus infection. Neutralizing antibody and interferon were not detectable in the early stage of the infection. These results suggested that polymorphonuclear leukocytes (Xray-sensitive, carrageenan-resistant) were the cells primarily responsible for early protection in influenza virus infection and that after infection with a high dose of the virus alveolar macrophages (X-ray-resistant, carrageenan-sensitive) also played a protective role in the early phase.

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“…This is because ECTV is naturally mouse adapted and expresses virulence factors, such as the IFN-␥ binding protein (28), that have greater affinity for the mouse than the VACV equivalents. It has been established that macrophages (20,43), NK cells (17), and CD8…”

Section: Genetic Resistance To Clinical Mousepox (Ectromelia Virus) Vmentioning

confidence: 99%

Expression of Mouse Interleukin-4 by a Recombinant Ectromelia Virus Suppresses Cytolytic Lymphocyte Responses and Overcomes Genetic Resistance to Mousepox

Jackson

Ramsay

Christensen

et al. 2001

J Virol

502

280

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Mechanism of Protection During the Early Phase of a Generalized Viral Infection. I. Contribution of Phagocytes to Protection against Ectromelia Virus

Cited by 23 publications

References 15 publications

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Protective Mechanisms against Pulmonary Infection with Influenza Virus. I. Relative Contribution of Polymorphonuclear Leukocytes and of Alveolar Macrophages to Protection during the Early Phase of Intranasal Infection

Expression of Mouse Interleukin-4 by a Recombinant Ectromelia Virus Suppresses Cytolytic Lymphocyte Responses and Overcomes Genetic Resistance to Mousepox

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