title: Dysregulation of allergic airway inflammation in the absence of microbial colonization.
abstract: BACKGROUND
  The incidence of allergic disorders is increasing in developed countries and has been associated with reduced exposure to microbes and alterations in the commensal bacterial flora.
  
  
  OBJECTIVE
  To ascertain the relevance of commensal bacteria on the development of an allergic response, we used a model of allergic airway inflammation in germ-free (GF) mice that lack any exposure to pathogenic or nonpathogenic microorganisms.
  
  
  METHODS
  Allergic airway inflammation was induced in GF, specific pathogen-free (SPF), or recolonized mice by sensitization and challenge with ovalbumin. The resulting cellular infiltrate and cytokine production were measured.
  
  
  RESULTS
  Our results show that the total number of infiltrating lymphocytes and eosinophils were elevated in the airways of allergic GF mice compared with control SPF mice, and that this increase could be reversed by recolonization of GF mice with the complex commensal flora of SPF mice. Exaggerated airway eosinophilia correlated with increased local production of Th2-associated cytokines, elevated IgE production, and an altered number and phenotype of conventional dendritic cells. Regulatory T-cell populations and regulatory cytokine levels were unaltered, but GF mice exhibited an increased number of basophils and decreased numbers of alveolar macrophages and plasmacytoid dendritic cells.
  
  
  CONCLUSIONS
  These data demonstrate that the presence of commensal bacteria is critical for ensuring normal cellular maturation, recruitment, and control of allergic airway inflammation.
authors.affiliation: Institute of Microbiology, Swiss Federal Institute of Technology, Zurich, Switzerland.
authors.forename: Tina
authors.initials: T
authors.lastname: Herbst
authors.forename: Anke
authors.initials: A
authors.lastname: Sichelstiel
authors.forename: Corinne
authors.initials: C
authors.lastname: Schär
authors.forename: Koshika
authors.initials: K
authors.lastname: Yadava
authors.forename: Kurt
authors.initials: K
authors.lastname: Bürki
authors.forename: Julia
authors.initials: J
authors.lastname: Cahenzli
authors.forename: Kathy
authors.initials: K
authors.lastname: McCoy
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Marsland
authors.forename: Nicola L
authors.initials: NL
authors.lastname: Harris
mesh_terms: D000818:Animals; D001249:Asthma / Q000150:complications / Q000276:immunology*; D001491:Basophils / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000276:immunology; D005434:Flow Cytometry; D007073:Immunoglobulin E / Q000276:immunology; D007249:Inflammation / Q000150:complications / Q000276:immunology*; D008168:Lung / Q000276:immunology*; D016676:Macrophages, Alveolar / Q000276:immunology; D054892:Metagenome / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin; D013047:Specific Pathogen-Free Organisms; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D007073:Immunoglobulin E; D010047:Ovalbumin