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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

Histopathological features of the brain cortex of WT and TNF-α KO mice infected with Oshima (a) and Sofjin (b) at 104 pfu and those of mock-infected mice (c).Sacrifice of mice was done at 9 days pi. Each figure represents three to five mice.
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f6: Histopathological features of the brain cortex of WT and TNF-α KO mice infected with Oshima (a) and Sofjin (b) at 104 pfu and those of mock-infected mice (c).Sacrifice of mice was done at 9 days pi. Each figure represents three to five mice.

Mentions: Following Oshima infection, TNF-α KO mice exhibited severe neuronal loss in several areas of the brain cortex when compared with WT mice (Figure 6a). Following Sofjin infection, more severe neuronal damage was observed in both of WT and TNF-α KO mice (Figure 6b). Accordingly, the degree of neuronal damage on Sofjin-infected WT and TNF-α KO mice was more extensive than that of Oshima-infected mice (Figure 6a and 6B). Mock-infected mice showed none of the neuronal destruction (Figure 6c). These observations suggest that severe neuronal damage indeed correlate with the increase in mortality and that TNF-α deficiency enhanced severe neuronal damage resulting in 100% mortality in TBEV-infected mice.


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)

Histopathological features of the brain cortex of WT and TNF-α KO mice infected with Oshima (a) and Sofjin (b) at 104 pfu and those of mock-infected mice (c).Sacrifice of mice was done at 9 days pi. Each figure represents three to five mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f6: Histopathological features of the brain cortex of WT and TNF-α KO mice infected with Oshima (a) and Sofjin (b) at 104 pfu and those of mock-infected mice (c).Sacrifice of mice was done at 9 days pi. Each figure represents three to five mice.
Mentions: Following Oshima infection, TNF-α KO mice exhibited severe neuronal loss in several areas of the brain cortex when compared with WT mice (Figure 6a). Following Sofjin infection, more severe neuronal damage was observed in both of WT and TNF-α KO mice (Figure 6b). Accordingly, the degree of neuronal damage on Sofjin-infected WT and TNF-α KO mice was more extensive than that of Oshima-infected mice (Figure 6a and 6B). Mock-infected mice showed none of the neuronal destruction (Figure 6c). These observations suggest that severe neuronal damage indeed correlate with the increase in mortality and that TNF-α deficiency enhanced severe neuronal damage resulting in 100% mortality in TBEV-infected mice.

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