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Protective role of TNF-α, IL-10 and IL-2 in mice infected with the Oshima strain of Tick-borne encephalitis virus.

Tun MM, Aoki K, Senba M, Buerano CC, Shirai K, Suzuki R, Morita K, Hayasaka D - Sci Rep (2014)

Bottom Line: Tick-borne encephalitis virus (TBEV) causes acute central nervous system disease.However, viral loads and proinflammatory cytokine levels in the brain of TNF-α KO andIL-10 KO mice were not significantly different compared with those of WT mice.From these results, we suggest that TNF-α, IL-10 and IL-2 are key factors for disease remission from fatal encephalitis due to infection with Oshima strain of TBEV.

View Article: PubMed Central - PubMed

Affiliation: Department of Virology, Institute of Tropical Medicine, Leading Graduate School Program, Nagasaki University, 852-8523, Nagasaki, Japan.

ABSTRACT
Tick-borne encephalitis virus (TBEV) causes acute central nervous system disease. Here, we investigated the roles of the TNF-α, IL-10 and other cytokines in appropriate KO mice following infection with Oshima and Sofjin strains of TBEV. Following infection with the Oshima strain, mortality rates were significantly increased in TNF-α KO and IL-10 KO mice compared with wild type (WT) mice. These results suggested that TNF-α and IL-10 play protective roles against fatal infection due to Oshima strain infection. However, viral loads and proinflammatory cytokine levels in the brain of TNF-α KO andIL-10 KO mice were not significantly different compared with those of WT mice. On the other hand, all WT, TNF-α KO and IL-10 KO mice died following infection with Sofjin strain. Interestingly, Sofjin-infected mice did not exhibit an up-regulated mRNA level of IL-2 in the spleen in all groups of mice, whereas Oshima-infected mice showed significantly increased level of IL-2 compared with mock-infected mice. From these results, we suggest that TNF-α, IL-10 and IL-2 are key factors for disease remission from fatal encephalitis due to infection with Oshima strain of TBEV.

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Related in: MedlinePlus

Viral loads in the spleen and CNS of WT, IL-10 KO and TNF-α KO mice (n = 4 to 10) at 5 and 9 days pi after subcutaneous infection with 104 pfu of Oshima (a) and Sofjin (b).
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f2: Viral loads in the spleen and CNS of WT, IL-10 KO and TNF-α KO mice (n = 4 to 10) at 5 and 9 days pi after subcutaneous infection with 104 pfu of Oshima (a) and Sofjin (b).

Mentions: Following infection with the Oshima strain, viral load in the spleen decreased at 9 days pi compared with at 5 days pi in all WT, IL-10 KO and TNF-α KO groups, whereas CNS infection increased during this period in all the groups (Figure 2a). However, there was no significant difference in the viral load in the spleen and in the CNS between the three groups at 5 days pi nor 9 days pi, suggesting that the increased mortality in IL-10 KO and TNF-α KO mice was not simply correlated with the increased viral loads in the peripheral and CNS tissues.


Protective role of TNF-α, IL-10 and IL-2 in mice infected with the Oshima strain of Tick-borne encephalitis virus.

Tun MM, Aoki K, Senba M, Buerano CC, Shirai K, Suzuki R, Morita K, Hayasaka D - Sci Rep (2014)

Viral loads in the spleen and CNS of WT, IL-10 KO and TNF-α KO mice (n = 4 to 10) at 5 and 9 days pi after subcutaneous infection with 104 pfu of Oshima (a) and Sofjin (b).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061546&req=5

f2: Viral loads in the spleen and CNS of WT, IL-10 KO and TNF-α KO mice (n = 4 to 10) at 5 and 9 days pi after subcutaneous infection with 104 pfu of Oshima (a) and Sofjin (b).
Mentions: Following infection with the Oshima strain, viral load in the spleen decreased at 9 days pi compared with at 5 days pi in all WT, IL-10 KO and TNF-α KO groups, whereas CNS infection increased during this period in all the groups (Figure 2a). However, there was no significant difference in the viral load in the spleen and in the CNS between the three groups at 5 days pi nor 9 days pi, suggesting that the increased mortality in IL-10 KO and TNF-α KO mice was not simply correlated with the increased viral loads in the peripheral and CNS tissues.

Bottom Line: Tick-borne encephalitis virus (TBEV) causes acute central nervous system disease.However, viral loads and proinflammatory cytokine levels in the brain of TNF-α KO andIL-10 KO mice were not significantly different compared with those of WT mice.From these results, we suggest that TNF-α, IL-10 and IL-2 are key factors for disease remission from fatal encephalitis due to infection with Oshima strain of TBEV.

View Article: PubMed Central - PubMed

Affiliation: Department of Virology, Institute of Tropical Medicine, Leading Graduate School Program, Nagasaki University, 852-8523, Nagasaki, Japan.

ABSTRACT
Tick-borne encephalitis virus (TBEV) causes acute central nervous system disease. Here, we investigated the roles of the TNF-α, IL-10 and other cytokines in appropriate KO mice following infection with Oshima and Sofjin strains of TBEV. Following infection with the Oshima strain, mortality rates were significantly increased in TNF-α KO and IL-10 KO mice compared with wild type (WT) mice. These results suggested that TNF-α and IL-10 play protective roles against fatal infection due to Oshima strain infection. However, viral loads and proinflammatory cytokine levels in the brain of TNF-α KO andIL-10 KO mice were not significantly different compared with those of WT mice. On the other hand, all WT, TNF-α KO and IL-10 KO mice died following infection with Sofjin strain. Interestingly, Sofjin-infected mice did not exhibit an up-regulated mRNA level of IL-2 in the spleen in all groups of mice, whereas Oshima-infected mice showed significantly increased level of IL-2 compared with mock-infected mice. From these results, we suggest that TNF-α, IL-10 and IL-2 are key factors for disease remission from fatal encephalitis due to infection with Oshima strain of TBEV.

Show MeSH
Related in: MedlinePlus