Abstract
Norovirus infection cause epidemic nonbacterial gastroenteritis in patients. The immune mechanisms responsible for the clearance of virus are not completely understood. We examined whether NKT cells are effective against norovirus infection using CD1d KO mice. The body weights of 4-weeks-old CD1d KO mice that were infected with murine norovirus-S7 (MNV-S7) were significantly lower than those of non-infected CD1d KO mice. On the other hand, the body weights of infected WT mice were comparable to those of non-infected WT mice. Correspondingly, CD1d KO mice had an almost 1000-fold higher MNV-S7 burden in the intestine after infection in comparison to WT mice. The mechanism responsible for the insufficient MNV-S7 clearance in CD1d KO mice was attributed to reduced IFN-γ production early during MNV-S7 infection. In addition, the markedly impaired IL-4 production in CD1d KO mice resulted in an impaired MNV-S7-specific secretory IgA production after MNV-S7 infection which is associated with mucosal immunity. Thus, the present results provide evidence that NKT cells play an essential role in MNV-S7 clearance.
Highlights
Human norovirus infection is the leading cause of seasonal epidemic non-bacterial gastroenteritis in patients of all ages
To evaluate whether NKT cells have a protective effect against murine norovirus-S7 (MNV-S7) infection, both WT mice and CD1d KO mice were orally infected with 5 × 105 pfu/mouse of Murine norovirus (MNV)-S7 at 4 weeks of age
We demonstrated that CD1d KO mice infected with MNV-S7 showed low body weight in comparison to non-infected CD1d KO mice
Summary
Human norovirus infection is the leading cause of seasonal epidemic non-bacterial gastroenteritis in patients of all ages. MNV is quickly cleared in WT mice, the viral infection is lethal in Stat1−/− mice, which cannot mediate IFNs-stimulated gene transcription signal pathway involving IFN-α, IFN-β and IFN-γ, in association with a high MNV titer burden in multiple tissues [2,3], We showed that IFN-α/β induced by lactoferin prevent MNV-S7 replication in vitro [4]. These reports imply that the IFNs signal pathway plays a major role in MNV clearance. Both IFN-γ and IFN-α/β play important roles in the clearance of MNV, because mice with the deletion of both IFN-γ receptor and IFN-α/
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