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The Journal of Neuroscience, October 8, 2008, 28(41):10330-10338; doi:10.1523/JNEUROSCI.2644-08.2008

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Neurobiology of Disease
Neuroprotective Effect of Apolipoprotein D against Human Coronavirus OC43-Induced Encephalitis in Mice

Sonia Do Carmo,^1 * Hélène Jacomy,^2 * Pierre J. Talbot,² and Eric Rassart¹

¹Laboratoire de Biologie Moléculaire, Département des Sciences Biologiques, and BioMed, Centre de Recherches Biomédicales, Université du Québec à Montréal, Montréal, Québec, Canada H3C 3P8, and ²Laboratory of Neuroimmunovirology, Institut National de la Recherche Scientifique–Institut Armand-Frappier, Laval, Québec, Canada H7V 1B7

Correspondence should be addressed to Eric Rassart, Département des Sciences Biologiques, Université du Québec à Montréal, Case Postale 8888, Succursale Centre-ville, Montréal, Québec, Canada H3C 3P8. Email: rassart.eric{at}uqam.ca

Apolipoprotein D (apoD) is a lipocalin upregulated in the nervous system after injury or pathologies such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. We previously demonstrated that apoD protects against neuropathology by controlling the level of peroxidated lipids. Here, we further investigated the biological function of apoD in a mouse model of acute encephalitis. Our results show that apoD transcript and protein are upregulated during acute encephalitis induced by the human coronavirus OC43 (HCoV-OC43) infection. The apoD upregulation coincides with glial activation, and its expression returns to normal levels when the virus is cleared, concomitantly to a resolved glial reactivity. In addition, the overexpression of human apoD in the neurons of Thy-1/ApoD transgenic mice results in a threefold increase of the number of mice surviving to HCoV-OC43 infection. This increased survival rate is correlated with an upregulated glial activation associated with a limited innate immune response (cytokines, chemokines) and T-cell infiltration into infected brains. Moreover, the protection seems to be associated with a restricted phospholipase A2 activity. These data reveal a role for apoD in the regulation of inflammation and suggest that it protects from HCoV-OC43-induced encephalitis, most likely through the phospholipase A2 signaling pathways.

Key words: apolipoprotein D; inflammation; viral encephalitis; phospholipase A2; T-cell infiltration; virus

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Received June 10, 2008; revised Aug. 26, 2008; accepted Aug. 30, 2008.

Correspondence should be addressed to Eric Rassart, Département des Sciences Biologiques, Université du Québec à Montréal, Case Postale 8888, Succursale Centre-ville, Montréal, Québec, Canada H3C 3P8. Email: rassart.eric{at}uqam.ca

This article has been cited by other articles:

				S. D. Carmo, D. Fournier, C. Mounier, and E. Rassart Human apolipoprotein D overexpression in transgenic mice induces insulin resistance and alters lipid metabolism Am J Physiol Endocrinol Metab, April 1, 2009; 296(4): E802 - E811. [Abstract] [Full Text] [PDF]

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