title: Differential expression of CCR3 ligand mRNA in guinea pig lungs during allergen-induced inflammation.
abstract: OBJECTIVE
  The gene expression profile of CCR3 ligands, eotaxin, RANTES, and monocyte chemoattractant protein-3 (MCP-3), was examined in normal and inflamed guinea pig lungs.
  
  
  METHODS
  Male Hartley guinea pigs (n = 49).
  
  
  METHODS
  Pulmonary mRNA was obtained from naive animals, animals treated with intravenous lipopolysaccharide administration, and animals repeatedly exposed to aerosolized allergen (ovalbumin). Northern analysis was performed to quantify pulmonary expression of eotaxin, RANTES, and MCP-3 mRNA. Pulmonary eosinophil peroxidase (EPO) activity was measured to quantify eosinophil accumulation.
  
  
  RESULTS
  Eotaxin and RANTES mRNAs, but not MCP-3 mRNA, were constitutively expressed in guinea pig lungs. Lipopolysaccharide treatment increased MCP-3 mRNA expression, but not eotaxin or RANTES mRNA. In contrast, allergen exposure in sensitized animals caused an increase in eotaxin mRNA, which demonstrated good temporal and quantitative correlation with pulmonary EPO activity, but not in MCP-3 or RANTES mRNA.
  
  
  CONCLUSIONS
  Guinea pig CCR3 ligands demonstrated different gene expression profiles in normal and inflamed airways, suggesting that they play different physiological and pathophysiological roles in the airway.
authors.affiliation: Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, Tokyo, Japan. ko-asano@qa2.so-net.ne.jp
authors.forename: K
authors.initials: K
authors.lastname: Asano
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Oguma
authors.forename: K
authors.initials: K
authors.lastname: Fukunaga
authors.forename: H
authors.initials: H
authors.lastname: Matsubara
authors.forename: T
authors.initials: T
authors.lastname: Shiomi
authors.forename: A
authors.initials: A
authors.lastname: Ishizaka
authors.forename: K
authors.initials: K
authors.lastname: Yamaguchi
authors.forename: M
authors.initials: M
authors.lastname: Kanazawa
mesh_terms: D000485:Allergens; D000818:Animals; D054413:Chemokine CCL11; D018946:Chemokine CCL5 / Q000096:biosynthesis; D054410:Chemokine CCL7; D019742:Chemokines, CC / Q000096:biosynthesis; D016207:Cytokines; D018076:DNA, Complementary / Q000096:biosynthesis / Q000235:genetics; D004804:Eosinophils / Q000201:enzymology; D006168:Guinea Pigs; D008168:Lung / Q000378:metabolism*; D008297:Male; D018945:Monocyte Chemoattractant Proteins / Q000096:biosynthesis; D010544:Peroxidases / Q000378:metabolism; D011014:Pneumonia / Q000139:chemically induced / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis*; D054397:Receptors, CCR3; D019707:Receptors, Chemokine / Q000096:biosynthesis*; D014158:Transcription, Genetic
chemical_list: D000485:Allergens; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D054410:Chemokine CCL7; D019742:Chemokines, CC; D016207:Cytokines; D018076:DNA, Complementary; D018945:Monocyte Chemoattractant Proteins; D012333:RNA, Messenger; D054397:Receptors, CCR3; D019707:Receptors, Chemokine; D010544:Peroxidases