title: Systemic eosinophil response induced by respiratory syncytial virus.
abstract: Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract disease (LRTD) in infants. Eosinophils have been suggested to play a role in the disease pathogenesis of LRTD. Inflammation can induce functional and morphological alterations of peripheral blood granulocytes. In patients with RSV LRTD, we aimed to investigate the eosinophil activation status by analysing surface markers. In vitro stimulation of eosinophils with cytokines leads to up-regulation of CD11b and priming markers recognized by the recently developed priming markers A17 and A27, whereas interleukin (IL)-5Ralpha is being down-regulated. In 51 patients and 10 controls we examined the expression of these surface markers on eosinophils in moderate to severe RSV-induced LRTD patients at the time of admission and 6 weeks later during the convalescence phase. RSV-patients were characterized by a higher eosinophil CD11b expression compared to controls. Although basal A17 and A27 expression was not increased, we observed a significantly higher expression of these priming epitopes on N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated cells of RSV patients compared with cells of controls, indicative of prior in vivo priming. Furthermore, IL-5Ralpha expression was down-regulated on peripheral blood eosinophils of these patients. Follow-up blood samples showed normalization of all markers but CD11b, which was persistently increased. Utilizing cellular markers, we observed that peripheral blood eosinophils from infants with RSV LRTD are in a more activated state compared to eosinophils of controls, which normalizes only partially during convalescence.
authors.affiliation: Department of Pulmonary Diseases, University Medical Centre, Utrecht, the Netherlands.
authors.forename: C A
authors.initials: CA
authors.lastname: Lindemans
authors.forename: J L L
authors.initials: JL
authors.lastname: Kimpen
authors.forename: B
authors.initials: B
authors.lastname: Luijk
authors.forename: J
authors.initials: J
authors.lastname: Heidema
authors.forename: D
authors.initials: D
authors.lastname: Kanters
authors.forename: C K
authors.initials: CK
authors.lastname: van der Ent
authors.forename: L
authors.initials: L
authors.lastname: Koenderman
mesh_terms: D000208:Acute Disease; D001990:Bronchiolitis, Viral / Q000276:immunology* / Q000628:therapy; D039481:CD11b Antigen / Q000097:blood; D002478:Cells, Cultured; D015536:Down-Regulation / Q000276:immunology; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D005500:Follow-Up Studies; D006760:Hospitalization; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D053666:Interleukin-5 Receptor alpha Subunit; D007958:Leukocyte Count; D008297:Male; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000276:immunology; D010102:Oxygen Inhalation Therapy; D018123:Receptors, Interleukin / Q000097:blood; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000628:therapy; D018113:Respiratory Syncytial Virus, Human
chemical_list: D039481:CD11b Antigen; C485918:IL5RA protein, human; D053666:Interleukin-5 Receptor alpha Subunit; D018123:Receptors, Interleukin; D009240:N-Formylmethionine Leucyl-Phenylalanine