Dengue virus-induced cytotoxin releases nitrite by spleen cells

Dengue type‐2 virus (DV) infection in mice induces T cells to produce a cytokine, the cytotoxic factor (CF), which induces H2‐A positive macrophages to produce another cytokine, cyotoxin (CF2), which amplifies its cytotoxic effects on target cells. The present study was undertaken to investigate the...

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Bibliographic Details
Published in:International journal of experimental pathology 1996-04, Vol.77 (2), p.45-51
Main Authors: MUKERJEE, RUMA, MISRA, ANITA, CHATURVEDI, U.C.
Format: Article
Language:English
Subjects:
Animals
Arginase - pharmacology
Arginine - analogs & derivatives
Arginine - pharmacology
Biological and medical sciences
Calcium - physiology
Cell Culture Techniques
Cytokines - immunology
cytotoxic cytokine
cytotoxicity
Cytotoxicity, Immunologic
Cytotoxins - antagonists & inhibitors
Cytotoxins - immunology
dengue virus
Dengue Virus - immunology
Dose-Response Relationship, Immunologic
Experimental viral diseases and models
Immune Sera
Infectious diseases
Medical sciences
Mice
Mice, Inbred Strains
Nitric Oxide - antagonists & inhibitors
nitrite
Nitrites - metabolism
omega-N-Methylarginine
Original
Proteins
Spleen - immunology
Sulfates - pharmacology
Viral diseases
Zinc Compounds - pharmacology
Zinc Sulfate
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Summary:Dengue type‐2 virus (DV) infection in mice induces T cells to produce a cytokine, the cytotoxic factor (CF), which induces H2‐A positive macrophages to produce another cytokine, cyotoxin (CF2), which amplifies its cytotoxic effects on target cells. The present study was undertaken to investigate the production of nitrite (NO−2) by the spleen cells of mice in vitro and in vivo following inoculation of CF2. Maximum NO−2 production occurred at 1 hour after inoculation of 100 μg CF2. Pretreatment of CF2 with anti‐CF2‐antisera (CF2‐As) inhibited the production of NO−2. Pretreatment of the spleen cells with NG‐monomethyl‐l‐arginine (NMA) or with arginase inhibited NO−2 production. The NO−2 production was diminished in a dose dependent manner by treatment of spleen cells with the Ca2+ channel blocking drug, nifedipine and Zn2+ as ZnSO4. The findings of the present study thus demonstrate that CF2 induces production of NO−2 in the spleen cells in a CA2+‐dependent manner which may be a mechanism of target cell killing.
ISSN:0959-9673
1365-2613
DOI:10.1046/j.1365-2613.1996.962100.x