title: Reovirus type-2 infection in newborn DBA/1J mice reduces the development of late allergic asthma.
abstract: The aim of the present study was to determine whether or not the development of a helper T (Th) 1 response induced by Reovirus type-2 (Reo-2) infection would protect against the development of Th2-mediated late allergic asthma. This hypothesis was examined by infecting one day old neonatal DB A/1J mice with Reo-2 in an ovalbumin (OVA)-induced late asthma model. Compared with the controls (either infected or uninfected mice with or without OVA sensitization and/or OVA challenge), Reo-2 infection lessened the magnitude of the subsequent allergic Th2-mediated late asthma. In infected mice with allergic late asthma, there was decreased infiltration of interleukin (IL)-4(+), IL-5(+), IL-13(+) and very late antigen (VLA)-4(+) lymphocytes, and eotaxin-2(+) and VLA-4(+) eosinophils, in both bronchial and bronchiolar lesions. Also the expression of vascular cell adhesion molecule (VCAM)-1 and eotaxin-2 on vascular endothelial cells was reduced. Moreover, the systemic production of IL-4, IL-5, tumour necrosis factor-α and OVA-specific IgE was reduced, whereas systemic IFN-γ production was increased. In addition, there was no increase in IFN-α production. Thus the present study suggests that systemic Reo-2 infection at birth may reduce the development of subsequent late allergic asthma by the induction of a Th1 response. Therefore the potential suppressive mechanism(s) that might be induced by Reo-2 infection in newborn mice and their effects on the development of late allergic asthma are discussed.
authors.affiliation: Laboratory of Veterinary Pathology, The United graduate School of Veterinary Science, Yamaguchi University, Yamaguchi, Japan.
authors.forename: Tomomi
authors.initials: T
authors.lastname: Nakashima
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Hayashi
authors.forename: Takuya
authors.initials: T
authors.lastname: Mizuno
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D000831:Animals, Newborn; D001249:Asthma / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D001980:Bronchi / Q000276:immunology* / Q000473:pathology; D016207:Cytokines / Q000276:immunology; D005260:Female; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D030102:Orthoreovirus, Mammalian / Q000276:immunology*; D012088:Reoviridae Infections / Q000276:immunology*
chemical_list: D000485:Allergens; D016207:Cytokines