title: Abnormal expressions of inflammatory-related mediators and inhibition of fat metabolism in mice infected with influenza a virus.
abstract: The pathophysiological role of influenza infection is poorly understood. In this study, one non-neurovirulent virus (IAV/Aichi/2/68/H3N2) strain was used to infect intra-nasally mice at different age to investigate the mechanism of cerebral edema formation and lower activities of mitochondria enzymes after influenza A virus (IAV) infection. Mice suffered 46.4% mortality in newborn compared with 96.0% in weanling, 100% in adult on day 7, respectively. IAV-RNA was easily detected in the brain of newborn mice. Significant production of endothelin-1 and inducible nitric oxide syntheses were increased on the 3rd and 5th day after IAV infection, associated with increasing blood-brain barrier permeability, brain edema formation and the higher mortality of animals. Production of tumor necrosis factor-α was related to inhibition of mitochondrial enzyme activities, suggesting that over expression of inflammatory cytokines and lower enzyme activities in mitochondria after IAV infection.
authors.affiliation: Department of Immunology, Medical School, Nantong University, Jiangsu, China.
authors.forename: Min
authors.initials: M
authors.lastname: Yao
authors.affiliation: Department of Medical informatics, MedicalSchool, Nantong University, Jiangsu, China.
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.affiliation: Key Lab. of Neuroregeneration, Nantong University, Jiangsu, China.
authors.forename: Dengbing
authors.initials: D
authors.lastname: Yao
authors.affiliation: Affiliated Hospitalof Nantong University, Jiangsu, China.
authors.forename: Dengfu
authors.initials: D
authors.lastname: Yao
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000276:immunology / Q000378:metabolism* / Q000821:virology; D001929:Brain Edema / Q000276:immunology / Q000378:metabolism* / Q000821:virology; D002199:Capillary Permeability; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000378:metabolism; D054884:Host-Pathogen Interactions; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism*; D009980:Influenza A virus / Q000235:genetics / Q000472:pathogenicity*; D050356:Lipid Metabolism; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000378:metabolism / Q000821:virology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D009976:Orthomyxoviridae Infections / Q000276:immunology / Q000378:metabolism* / Q000821:virology; D012367:RNA, Viral / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019562:Viral Load
chemical_list: D019332:Endothelin-1; D018836:Inflammation Mediators; D012367:RNA, Viral; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse