title: Prostaglandin E2 production during neonatal respiratory infection with mouse adenovirus type 1.
abstract: Neonatal mice are more susceptible than adults to mouse adenovirus type 1 (MAV1) respiratory infection. In adult mice, MAV-1 respiratory infection induces production of prostaglandin E2 (PGE2), a lipid mediator that exerts suppressive effects on a variety of host immune functions. We tested the hypothesis that exaggerated PGE2 production in neonatal mice contributes to increased susceptibility to MAV-1. PGE2 concentrations were lower in lungs of uninfected neonatal mice than in adults. PGE2 production was induced by both MAV-1 and a nonspecific stimulus to a greater degree in neonatal mice than in adults, but only in adults was PGE2 induced in a virus-specific manner. Lung viral loads were equivalent in PGE2-deficient neonatal mice and wild type controls, as was virus-induced expression of IFN-γ, IL-17A, and CCL5 in the lungs. PGE2 deficiency had minimal effect on production of virus-specific IgG or establishment of protective immunity in neonatal mice. Collectively, our data indicate that lung PGE2 production is exaggerated early in life, but this effect does not mediate increased susceptibility to MAV-1 infection.
authors.affiliation: Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States.
authors.forename: Megan C
authors.initials: MC
authors.lastname: Procario
authors.affiliation: Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, United States.
authors.forename: Mary K
authors.initials: MK
authors.lastname: McCarthy
authors.affiliation: Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States.
authors.forename: Rachael E
authors.initials: RE
authors.lastname: Levine
authors.affiliation: Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States.
authors.forename: Caitlyn T
authors.initials: CT
authors.lastname: Molloy
authors.affiliation: Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, United States. Electronic address: jbwein@umich.edu.
authors.forename: Jason B
authors.initials: JB
authors.lastname: Weinberg
mesh_terms: D056704:Adaptive Immunity; D000256:Adenoviridae; D000257:Adenoviridae Infections / Q000235:genetics / Q000378:metabolism* / Q000821:virology*; D000818:Animals; D000831:Animals, Newborn; D000914:Antibodies, Viral / Q000276:immunology; D000918:Antibody Specificity / Q000276:immunology; D002460:Cell Line; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism*; D015870:Gene Expression; D008168:Lung / Q000378:metabolism / Q000473:pathology / Q000821:virology; D051379:Mice; D018345:Mice, Knockout; D018078:Receptors, Prostaglandin E / Q000235:genetics / Q000378:metabolism; D012141:Respiratory Tract Infections / Q000235:genetics / Q000378:metabolism* / Q000821:virology*; D019562:Viral Load
chemical_list: D000914:Antibodies, Viral; D016207:Cytokines; D018078:Receptors, Prostaglandin E; D015232:Dinoprostone
keywords: Adenovirus; Neonatal infection; Prostaglandin E(2); Viral pathogenesis