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The resistance against Trichinella spiralis infection induced by primary infection with respiratory syncytial virus

Published online by Cambridge University Press:  05 November 2018

Ki-Back Chu
Affiliation:
Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul, Korea
Dong-Hun Lee
Affiliation:
Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul, Korea
Hae-Ji Kang
Affiliation:
Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul, Korea
Fu-Shi Quan*
Affiliation:
Department of Medical Zoology, Kyung Hee University School of Medicine, Seoul, Korea Biomedical Science Institute, Kyung Hee University, Seoul, Korea
*
Author for correspondence: Fu-Shi Quan, E-mail: [email protected]

Abstract

Human infections with Trichinella spiralis and respiratory syncytial virus (RSV) are common, as T. spiralis infections are re-emerging in various parts of the world and RSV infections remain a threat for infants. Yet, studies investigating the relationship pertaining to the two are severely lacking. In particular, immune response induction via RSV and T. spiralis remain largely elusive. Here, we investigated the resistance against T. spiralis infection induced upon primary infection with RSV. RSV, notorious for causing severe inflammatory reaction in the lungs, were intranasally infected, followed with a T. spiralis infection in mice. Our results revealed that primary RSV infection in mice significantly raised T. spiralis-specific and total IgE, IgG and its subclass antibody responses upon T. spiralis challenge infection (RSV-Ts). Blood eosinophil levels were decreased in RSV-Ts, accompanied with significant increase in both Th1 and Th2 cytokines. Antibodies generated against RSV in RSV-infected mice were found to react with T. spiralis excretory/secretory antigen, showing several bands determined through immunoblotting. RSV-Ts also had a marked reduction of T. spiralis worm burden in diaphragm. These results indicate that immune responses induced by RSV infection contribute to resistance against subsequent T. spiralis infection.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2018 

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