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Upregulated Expression of Iba1 Molecules in the Central Nervous System of Mice in Response to Neurovirulent Influenza A Virus Infection
Author(s) -
Mori Isamu,
Imai Yoshinori,
Kohsaka Shinichi,
Kimura Yoshinobu
Publication year - 2000
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2000.tb02556.x
Subject(s) - microglia , biology , virus , olfactory bulb , central nervous system , influenza a virus , virology , downregulation and upregulation , immunology , microbiology and biotechnology , neuroscience , gene , inflammation , genetics
The present study deals with the expression of Ibal molecules, a novel EF‐hand Ca 2+ ‐binding protein, in the brain after stereotaxic introduction of the neurovirulent WSN strain of influenza A virus into the olfactory bulb of C57BL/6 mice. The virus selectively targeted the paraventricular and anterior olfactory nuclei. Infected neurons appeared as early as at day 3 post infection and degenerated and vanished by day 12. The Ibal molecule was normally expressed in resting microglia. The overexpression of the Ibal in microglial cells was detected at day 3 post infection, culminating at day 7 with a morphological activation. Ibal‐immunopositive macrophages outnumbered microglia in the paraventricular and anterior olfactory nuclei, where the infected neurons had degenerated. Macrophages totally disappeared by day 12, and the Ibal‐expression in microglia was reduced to a normal level by day 35. Lack of perforin predisposed the mice to long‐term virus infection of the brain, leading to the prolonged Ibal‐overexpression. These results show that the Ibal is upregulated in the mouse brain in response to influenza virus infection and may play significant roles in the regulation of some immunological and pathophysiological functions of microglia during virus infection.