title: Eosinophilic apoptosis in sinus mucosa: relationship to tissue eosinophilia and its resolution in allergic sinusitis.
abstract: BACKGROUND
  Apoptosis, which is regulated by both cell survival and death signals, is important for the swift clearance of unwanted cells.
  
  
  OBJECTIVE
  We sought to elucidate whether eosinophilic apoptosis is associated with tissue eosinophilia and to determine its resolution in allergic sinusitis (AS).
  
  
  METHODS
  Numbers of eosinophils, numbers of IL-5(+) cells, and the apoptosis index of eosinophils were calculated in the submucosa (both superficial and deep layers) of patients with AS by using histochemical methods before and after prednisolone treatment. Patients without AS were used for control groups. Anti-EG2 antibody was used to identify eosinophils. IL-5, Fas, or Bax expression of eosinophils was evaluated to elucidate the role of the factors affecting eosinophilic apoptosis.
  
  
  RESULTS
  EG2 and IL-5(+) cells were abundant in the submucosa of patients with AS, especially in the superficial layer. About 50% to 60% of the IL-5-producing cells were eosinophils. Apoptotic eosinophils were less numerous in the superficial layer than the deep layer in these diseases. After prednisolone treatment, an induction of eosinophilic apoptosis was accompanied by a significant decrease in the number of EG2(+) and IL-5(+) cells. No remarkable difference was observed in the Fas or Bax expression of eosinophils after prednisolone treatment.
  
  
  CONCLUSIONS
  Autocrine secretion of IL-5 from eosinophils may be one reason why eosinophilic disease is difficult to manage. Induction of eosinophilic apoptosis is critical for reversing tissue eosinophilia in patients with AS.
authors.affiliation: Department of Otorhinolaryngology, Osaka Medical College, Osaka, Japan.
authors.forename: G K
authors.initials: GK
authors.lastname: Fan
authors.forename: T
authors.initials: T
authors.lastname: Itoh
authors.forename: M
authors.initials: M
authors.lastname: Imanaka
authors.forename: S
authors.initials: S
authors.lastname: Fujieda
authors.forename: H
authors.initials: H
authors.lastname: Takenaka
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000293:Adolescent; D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D051017:Apoptosis Regulatory Proteins; D002352:Carrier Proteins / Q000096:biosynthesis; D004802:Eosinophilia / Q000473:pathology*; D004804:Eosinophils / Q000737:chemistry / Q000166:cytology / Q000378:metabolism; D015521:Ethmoid Sinusitis / Q000276:immunology* / Q000378:metabolism; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000175:diagnosis / Q000378:metabolism; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D015848:Interleukin-5 / Q000096:biosynthesis / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D015523:Maxillary Sinusitis / Q000276:immunology* / Q000378:metabolism; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D051017:Apoptosis Regulatory Proteins; C494826:BAX protein, human; D002352:Carrier Proteins; C490780:FAF1 protein, human; D015848:Interleukin-5; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D011239:Prednisolone