title: Eosinophil influx to the nasal airway after local, low-level LPS challenge in humans.
abstract: BACKGROUND
  Recent observations show that atopic asthmatic subjects have increased sensitivity to respirable endotoxin (or LPS) compared with normal persons. In vitro studies demonstrate that LPS enhances eosinophil survival. These observations suggest that the effects of inhaled LPS in asthmatic subjects may include increases in the number of airway eosinophils.
  
  
  OBJECTIVE
  We sought to determine whether low-level nasal LPS challenge causes an increase in eosinophil numbers in the nasal airways of atopic or normal subjects.
  
  
  METHODS
  Sixteen volunteers (10 atopic asthmatic subjects and 6 normal subjects) underwent 2 nasal challenge sessions. In one session, one nostril was challenged with saline and the other with 0. 1 microg of LPS. During the second session, 0.3 microg and 1.0 microg of LPS was delivered to each nostril, respectively. Nasal lavage fluid was obtained from each nostril before challenge, as well as 4 and 24 hours after challenge, and examined for the percent of total cells that were eosinophils and neutrophils, as well as cytokine levels.
  
  
  RESULTS
  LPS (1.0 microg) increased the percent of eosinophils in nasal lavage fluid 4 hours after challenge in atopic subjects only. There was also a correlation between constitutive nasal GM-CSF and eosinophil response to LPS in atopic subjects.
  
  
  CONCLUSIONS
  LPS challenge increases eosinophils in the airways of atopic subjects.
authors.affiliation: Center for Environmental Medicine and Lung Biology, the Department of Pediatrics, University of North Carolina School of Medicine, Chapel Hill 27599-7310, USA.
authors.forename: D B
authors.initials: DB
authors.lastname: Peden
authors.forename: K
authors.initials: K
authors.lastname: Tucker
authors.forename: P
authors.initials: P
authors.lastname: Murphy
authors.forename: L
authors.initials: L
authors.lastname: Newlin-Clapp
authors.forename: B
authors.initials: B
authors.lastname: Boehlecke
authors.forename: M
authors.initials: M
authors.lastname: Hazucha
authors.forename: P
authors.initials: P
authors.lastname: Bromberg
authors.forename: W
authors.initials: W
authors.lastname: Reed
mesh_terms: D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000473:pathology; D001798:Blood Proteins / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000166:cytology*; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006098:Granulocytes / Q000166:cytology; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000737:chemistry / Q000166:cytology*; D009299:Nasal Provocation Tests; D010865:Pilot Projects; D012260:Ribonucleases
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D016209:Interleukin-8; D008070:Lipopolysaccharides; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D012260:Ribonucleases