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J Gen Virol 68 (1987), 425-432; DOI 10.1099/0022-1317-68-2-425
© 1987 Society for General Microbiology

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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

Haruo Fujisawa, Sumiaki Tsuru, Mariko Taniguchi, Yutaka Zinnaka and Kikuo Nomoto1

Department of Microbiology, National Defense Medical College, Tokorozawa, Saitama 359
and1 Department of Immunology, Medical Institute for Bioregulation Research, Kyushu University, Fukuoka 812, Japan

The 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 103 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 104 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 (X-ray-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.

Keywords: influenza A virus, PMN, alveolar macrophages, early protection

Received 21 May 1986; accepted 24 October 1986.


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