title: Corticosteroid treatment ameliorates acute lung injury induced by 2009 swine origin influenza A (H1N1) virus in mice.
abstract: BACKGROUND
  The 2009 influenza pandemic affected people in almost all countries in the world, especially in younger age groups. During this time, the debate over whether to use corticosteroid treatment in severe influenza H1N1 infections patients resurfaced and was disputed by clinicians. There is an urgent need for a susceptible animal model of 2009 H1N1 infection that can be used to evaluate the pathogenesis and the therapeutic effect of corticosteroid treatment during infection.
  
  
  RESULTS
  We intranasally inoculated two groups of C57BL/6 and BALB/c mice (using 4- or 6-to 8-week-old mice) to compare the pathogenesis of several different H1N1 strains in mice of different ages. Based on the results, a very susceptible 4-week-old C57BL/6 mouse model of Beijing 501 strain of 2009 H1N1 virus infection was established, showing significantly elevated lung edema and cytokine levels compared to controls. Using our established animal model, the cytokine production profile and lung histology were assessed at different times post-infection, revealing increased lung lesions in a time-dependent manner. In additional,the mice were also treated with dexamethasone, which significantly improved survival rate and lung lesions in infected mice compared to those in control mice. Our data showed that corticosteroid treatment ameliorated acute lung injury induced by the 2009 A/H1N1 virus in mice and suggested that corticosteroids are valid drugs for treating 2009 A/H1N1 infection.
  
  
  CONCLUSIONS
  Using the established, very susceptible 2009 Pandemic Influenza A (H1N1) mouse model, our studies indicate that corticosteroids are a potential therapeutic remedy that may address the increasing concerns over future 2009 A/H1N1 pandemics.
authors.affiliation: Institute of Basic Medical Sciences, Department of Biochemistry and Molecular Biology, Peking Union Medical College, Tsinghua University, Beijing, China.
authors.forename: Chenggang
authors.initials: C
authors.lastname: Li
authors.forename: Penghui
authors.initials: P
authors.lastname: Yang
authors.forename: Yanli
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yang
authors.initials: Y
authors.lastname: Sun
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Zhen
authors.initials: Z
authors.lastname: Zou
authors.forename: Li
authors.initials: L
authors.lastname: Xing
authors.forename: Zhongwei
authors.initials: Z
authors.lastname: Chen
authors.forename: Chong
authors.initials: C
authors.lastname: Tang
authors.forename: Feng
authors.initials: F
authors.lastname: Guo
authors.forename: Jiejie
authors.initials: J
authors.lastname: Deng
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Yiwu
authors.initials: Y
authors.lastname: Yan
authors.forename: Jun
authors.initials: J
authors.lastname: Tang
authors.forename: Xiliang
authors.initials: X
authors.lastname: Wang
authors.forename: Chengyu
authors.initials: C
authors.lastname: Jiang
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology / Q000821:virology*; D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D004195:Disease Models, Animal; D007249:Inflammation / Q000150:complications / Q000473:pathology / Q000821:virology; D053118:Influenza A Virus, H1N1 Subtype / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009976:Orthomyxoviridae Infections / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology / Q000821:virology*; D034421:Sus scrofa / Q000821:virology*; D014886:Weaning
chemical_list: D000305:Adrenal Cortex Hormones; D016207:Cytokines; D003907:Dexamethasone