title: Eosinophils do not enhance the trans-basement-membrane migration of neutrophils.
abstract: BACKGROUND
  There is increasing evidence that both neutrophilic and eosinophilic inflammation persist in the airways of patients with severe asthma. We have reported a positive relationship between the concentrations of eosinophils and neutrophils in sputum from severe asthmatics, suggesting a possible role of eosinophils in regulating neutrophilic inflammation. The aim of this study was to investigate whether activated eosinophils modify the trans-basement membrane migration (TBM) of neutrophils.
  
  
  METHODS
  Eosinophils and neutrophils were isolated from peripheral blood drawn from healthy donors. The TBM of neutrophils in response to a variety of chemoattractants was evaluated in the presence or absence of eosinophils by using the chambers with a Matrigel-coated Transwell insert.
  
  
  RESULTS
  As expected, eotaxin (10 nM) and RANTES (10 nM), but not IL-8 (10 nM), induced the TBM of eosinophils. On the contrary, only IL-8 induced the TBM of neutrophils. When eosinophils were coincubated with neutrophils and stimulated with IL-8, the TBM of eosinophils was significantly augmented. On the other hand, when neutrophils were coincubated with eosinophils and stimulated with eotaxin or RANTES, the TBM of neutrophils was not modified.
  
  
  CONCLUSIONS
  Neutrophils migrated by IL-8 may lead eosinophils to accumulate in the airways of patients with severe asthma. On the other hand, it is unlikely that eosinophils migrated by chemoattractants such as CC chemokines regulate neutrophilic inflammation.
authors.affiliation: Department of Respiratory Medicine, Saitama Medical University, Iruma-gun, Saitama, Japan.
authors.forename: Takehito
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Yotaro
authors.initials: Y
authors.lastname: Takaku
authors.forename: Izumi
authors.initials: I
authors.lastname: Kikuchi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Soma
authors.forename: Koichi
authors.initials: K
authors.lastname: Hagiwara
authors.forename: Minoru
authors.initials: M
authors.lastname: Kanazawa
authors.forename: Makoto
authors.initials: M
authors.lastname: Nagata
mesh_terms: D000328:Adult; D001249:Asthma / Q000473:pathology; D001485:Basement Membrane; D002478:Cells, Cultured / Q000502:physiology; D054413:Chemokine CCL11; D018946:Chemokine CCL5 / Q000494:pharmacology; D019742:Chemokines, CC / Q000494:pharmacology; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D004804:Eosinophils / Q000502:physiology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D016209:Interleukin-8 / Q000494:pharmacology; D007975:Leukotriene B4 / Q000494:pharmacology; D008297:Male; D009504:Neutrophils / Q000502:physiology*; D011657:Pulmonary Eosinophilia / Q000503:physiopathology
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D019742:Chemokines, CC; D016209:Interleukin-8; D007975:Leukotriene B4