An insufficient anti-inflammatory cytokine response in mouse brain is associated with increased tissue pathology and viral load during Japanese encephalitis virus infection
Identifieur interne : 002C74 ( Main/Exploration ); précédent : 002C73; suivant : 002C75An insufficient anti-inflammatory cytokine response in mouse brain is associated with increased tissue pathology and viral load during Japanese encephalitis virus infection
Auteurs : V. Saxena [Inde] ; A. Mathur [Inde] ; N. Krishnani [Inde] ; T. N. Dhole [Inde]Source :
- Archives of Virology [ 0304-8608 ] ; 2008-02-01.
Abstract
Summary: Infection of the central nervous system with Japanese encephalitis virus (JEV) results in fatal encephalitis in humans. No reports exist describing the sequence of pathological changes and their correlation to the immune response in the brain following infection with JEV. In this report, we analyzed inducible nitric oxide synthase (iNOS) mRNA, proinflammatory (IFN-γ, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokine expression, viral load, and the correlation of these factors with the major histopathological changes in brain of JEV challenged mice at different time points during infection. We report for the first time that in JE, there is a progressive decline in the level of IL-4. The extent of progressive decrease in IL-4 and IL-10 level following viral infection is inversely correlated to the increased level of proinflammatory cytokines and histopathological changes with negative consequences following viral infection. In contrast, proinflammatory mediators like IFN-γ and TNF-α were significantly upregulated (P < 0.05). A negative correlation between IFN-γ and iNOS indicates their independent actions during JEV infection. To conclude, an insufficient anti-inflammatory cytokine response indicated by IL-4 and IL-10 in the brain is associated with increased tissue pathology and viral load, which regulates inflammatory responses driven by IFN-γ in concert with TNF-α to cause brain tissue damage.
Url:
DOI: 10.1007/s00705-007-1098-7
Affiliations:
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Saxena</name><affiliation wicri:level="1"><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow</wicri:regionArea><wicri:noRegion>Lucknow</wicri:noRegion></affiliation></author><author><name sortKey="Mathur, A" sort="Mathur, A" uniqKey="Mathur A" first="A." last="Mathur">A. Mathur</name><affiliation wicri:level="1"><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Microbiology, Saraswati Medical and Dental College, Lucknow</wicri:regionArea><wicri:noRegion>Lucknow</wicri:noRegion></affiliation></author><author><name sortKey="Krishnani, N" sort="Krishnani, N" uniqKey="Krishnani N" first="N." last="Krishnani">N. 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Dhole</name><affiliation wicri:level="1"><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow</wicri:regionArea><wicri:noRegion>Lucknow</wicri:noRegion></affiliation><affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Archives of Virology</title><title level="j" type="sub">Official Journal of the Virology Division of the International Union of Microbiological Societies</title><title level="j" type="abbrev">Arch Virol</title><idno type="ISSN">0304-8608</idno><idno type="eISSN">1432-8798</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="2008-02-01">2008-02-01</date><biblScope unit="volume">153</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="283">283</biblScope><biblScope unit="page" to="292">292</biblScope></imprint><idno type="ISSN">0304-8608</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0304-8608</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Infection of the central nervous system with Japanese encephalitis virus (JEV) results in fatal encephalitis in humans. No reports exist describing the sequence of pathological changes and their correlation to the immune response in the brain following infection with JEV. In this report, we analyzed inducible nitric oxide synthase (iNOS) mRNA, proinflammatory (IFN-γ, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokine expression, viral load, and the correlation of these factors with the major histopathological changes in brain of JEV challenged mice at different time points during infection. We report for the first time that in JE, there is a progressive decline in the level of IL-4. The extent of progressive decrease in IL-4 and IL-10 level following viral infection is inversely correlated to the increased level of proinflammatory cytokines and histopathological changes with negative consequences following viral infection. In contrast, proinflammatory mediators like IFN-γ and TNF-α were significantly upregulated (P < 0.05). A negative correlation between IFN-γ and iNOS indicates their independent actions during JEV infection. To conclude, an insufficient anti-inflammatory cytokine response indicated by IL-4 and IL-10 in the brain is associated with increased tissue pathology and viral load, which regulates inflammatory responses driven by IFN-γ in concert with TNF-α to cause brain tissue damage.</div></front></TEI><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Saxena, V" sort="Saxena, V" uniqKey="Saxena V" first="V." last="Saxena">V. Saxena</name></noRegion><name sortKey="Dhole, T N" sort="Dhole, T N" uniqKey="Dhole T" first="T. N." last="Dhole">T. N. Dhole</name><name sortKey="Krishnani, N" sort="Krishnani, N" uniqKey="Krishnani N" first="N." last="Krishnani">N. Krishnani</name><name sortKey="Mathur, A" sort="Mathur, A" uniqKey="Mathur A" first="A." last="Mathur">A. 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