title: Lung-derived SSEA-1(+) stem/progenitor cells inhibit allergic airway inflammation in mice.
abstract: BACKGROUND
  Asthma is characterized by chronic airway inflammation and airway hyperresponsiveness (AHR). Little is known about the role of pulmonary stem/progenitor cells (PSCs) in allergic airway inflammation.
  
  
  METHODS
  To identify and investigate the role of PSCs in the bronchial epithelium of neonatal mice, we developed an enzyme-based digestion method to obtain single-cell suspension from lung tissues. Characterization of PSCs was performed using flow cytometry, real-time PCR, immunofluorescence staining, confocal microscopy, and scanning electron microscopy. The effects of SSEA-1(+) (stage-specific embryonic antigen-1) PSCs was studied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of cell-based regulation using flow cytometry, real-time PCR, and immune-blotting.
  
  
  RESULTS
  Single-cell suspensions derived from neonatal lung tissue included populations that expressed either SSEA-1(+) or Sca-1(+) (stem cell antigen-1). The SSEA-1(+) PSCs were highly prevalent in neonatal mice, and they were rare in adult mice. Enriched neonatal SSEA-1(+) PSCs had the ability of self-renewal and differentiated into pneumocytes and tracheal epithelial cells. SSEA-1(+) PSCs reduced AHR and airway damage in asthmatic mice by decreasing eosinophil infiltration, inhibiting chemokines/cytokines production, and preserving the level of CCSP.
  
  
  CONCLUSIONS
  Here, we demonstrated that neonatal SSEA-1(+) PSCs play an immunomodulatory role in the progression of asthma by reducing lung damage and inhibiting inflammatory responses. Further understanding the molecular mechanisms of neonatal SSEA-1(+) PSCs might shed light on exploring the novel therapeutic approaches for allergic airway inflammation.
authors.affiliation: Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: C J
authors.initials: CJ
authors.lastname: Chiu
authors.forename: T Y
authors.initials: TY
authors.lastname: Ling
authors.forename: B L
authors.initials: BL
authors.lastname: Chiang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000066673:Cell Self Renewal; D019742:Chemokines, CC / Q000096:biosynthesis; D060965:Clonal Evolution; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D016130:Immunophenotyping; D016256:Lewis X Antigen / Q000378:metabolism*; D008168:Lung / Q000166:cytology* / Q000378:metabolism*; D051379:Mice; D039902:Multipotent Stem Cells / Q000166:cytology / Q000378:metabolism; D010641:Phenotype; D012130:Respiratory Hypersensitivity / Q000175:diagnosis / Q000276:immunology* / Q000378:metabolism* / Q000628:therapy; D020545:Respiratory Mucosa / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D012720:Severity of Illness Index; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D000094632:Thymic Stromal Lymphopoietin
chemical_list: D019742:Chemokines, CC; D016207:Cytokines; D016256:Lewis X Antigen; D000094632:Thymic Stromal Lymphopoietin; C000721967:TSLP protein, mouse
keywords: airway inflammation; asthma; pulmonary stem/progenitor cell