title: Leptin has a priming effect on eotaxin-induced human eosinophil chemotaxis.
abstract: BACKGROUND
  Tissue eosinophilia is one of the hallmarks of allergic diseases and Th2-type immune responses including asthma. Systemic inflammation caused by adipose tissue in obesity via production of adipokines such as leptin has been attracting attention recently as a contributor to exacerbation of allergic immune reactions. In this study, we examined whether leptin might affect eosinophil chemotactic responses.
  
  
  METHODS
  Peripheral blood eosinophils were purified, and the effect of leptin on eosinophil migration was investigated using in vitro systems.
  
  
  RESULTS
  High concentrations of leptin induced eosinophil chemotaxis and rapid phosphorylation of ERK1/2 and p38 mitogen-activated protein kinase but not calcium mobilization. We also found that pretreatment of eosinophils with physiological concentrations of leptin amplified the chemotactic responses to eotaxin. This leptin-primed chemotaxis appears to be associated with increased calcium mobilization but not with ERK1/2 and p38 pathways.
  
  
  CONCLUSIONS
  These results indicate that leptin has both direct and indirect effects on eosinophil chemotaxis and intracellular signaling. In physiological settings, leptin may maintain eosinophil accumulation at allergic inflammatory foci.
authors.affiliation: Department of Infection, Allergy, Clinical Immunology and Laboratory Medicine, Akita University Graduate School of Medicine, Akita, Japan.
authors.forename: Hikari
authors.initials: H
authors.lastname: Kato
authors.forename: Shigeharu
authors.initials: S
authors.lastname: Ueki
authors.forename: Rie
authors.initials: R
authors.lastname: Kamada
authors.forename: Junko
authors.initials: J
authors.lastname: Kihara
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Yamauchi
authors.forename: Tomomi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Masahide
authors.initials: M
authors.lastname: Takeda
authors.forename: Masamichi
authors.initials: M
authors.lastname: Itoga
authors.forename: Mami
authors.initials: M
authors.lastname: Chihara
authors.forename: Wataru
authors.initials: W
authors.lastname: Ito
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kayaba
authors.forename: Junichi
authors.initials: J
authors.lastname: Chihara
mesh_terms: D054413:Chemokine CCL11 / Q000276:immunology* / Q000494:pharmacology*; D002634:Chemotaxis, Leukocyte; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D006801:Humans; D020738:Leptin / Q000494:pharmacology* / Q000502:physiology*; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D010766:Phosphorylation; D011994:Recombinant Proteins / Q000494:pharmacology; D015398:Signal Transduction; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D020738:Leptin; D011994:Recombinant Proteins; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases