title: Grain dust and endotoxin inhalation challenges produce similar inflammatory responses in normal subjects.
abstract: OBJECTIVE
  To compare the physiologic and inflammatory response following inhalation of corn dust extract (CDE) and lipopolysaccharide (LPS) solutions in normal subjects.
  
  
  METHODS
  Randomized, double-blind crossover design.
  
  
  METHODS
  Fourteen healthy, nonatopic, nonasthmatic, never-smoking volunteers.
  
  
  METHODS
  On separate visits, subjects underwent a series of four inhalation challenges to LPS or CDE, each containing either a high (6 micrograms/mL) or low (0.9 microgram/mL) endotoxin concentration, and administered at equal Xolumes.
  
  
  RESULTS
  Chest tightness, cough, dyspnea, and sputum production were experienced following both LPS and CDE exposures and with similar frequency at both high and low endotoxin concentrations. LPS and CDE inhalations caused acute declines in FEV1, and the changes in FEV1 from baseline following exposure to both inhalants were not significantly different at both high and low endotoxin concentrations. Following exposure to the high-endotoxin LPS and CDE, no consistent differences in total cell and cytokine (tumor necrosis factor-alpha [TNF-alpha], interleukin-1 beta [IL-1 beta], IL-6, IL-8) concentrations were seen between exposures, although the neutrophil concentration was greater following the LPS exposure (p = 0.01). BAL cellularity and cytokine concentrations following the low-endotoxin LPS and CDE exposure revealed no differences, except for IL-1 beta, which was greater following LPS exposure (p = 0.05). The high-endotoxin LPS and CDE exposures resulted in greater increases in BAL neutrophils and cytokines in comparison to its respective low-endotoxin exposure.
  
  
  CONCLUSIONS
  At exposure levels of endotoxin, LPS and CDE result in similar symptoms, changes in airflow, and increases in BAL inflammatory cells and mediators. Moreover, the physiologic and inflammatory response to LPS and CDE appears to be related to the exposure level of endotoxin.
authors.affiliation: Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, USA.
authors.forename: P J
authors.initials: PJ
authors.lastname: Jagielo
authors.forename: P S
authors.initials: PS
authors.lastname: Thorne
authors.forename: J L
authors.initials: JL
authors.lastname: Watt
authors.forename: K L
authors.initials: KL
authors.lastname: Frees
authors.forename: T J
authors.initials: TJ
authors.lastname: Quinn
authors.forename: D A
authors.initials: DA
authors.lastname: Schwartz
mesh_terms: D000328:Adult; D001980:Bronchi / Q000473:pathology; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004391:Dust / Q000009:adverse effects*; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation; D016209:Interleukin-8 / Q000032:analysis; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D012140:Respiratory Tract Diseases / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D003313:Zea mays
chemical_list: D004391:Dust; D016209:Interleukin-8; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha