title: Interleukin-5 expression in the bone marrow of sensitized Balb/c mice after allergen challenge.
abstract: Interleukin-5 (IL-5) is a potent eosinophilopoietic factor implicated in the chronic inflammatory cell accumulation accompanying bronchial asthma. However, its role in stimulating eosinophil differentiation within the bone marrow following allergen exposure remains to be elucidated. The aims of our study were to determine the expression of IL-5 within the bone marrow of sensitized and control mice after allergen exposure, and to investigate the cellular phenotype of IL-5-producing cells. Sensitized Balb/c mice were challenged with either ovalbumin (OVA) or sterile saline. After 6 h, the mice were exsanguinated and the bone marrow prepared for cytospins. Bone marrow-derived cells from OVA-sensitized mice exhibited an increase in IL-5 immunoreactivity and mRNA compared with those from nonsensitized control mice (p < 0. 05). After allergen challenge, there was a further increase in IL-5 expression (p < 0.05) within the bone marrow. Both sensitization and allergen challenge resulted in an increase in the number of cells expressing major basic protein (MBP) (p < 0.05). In nonsensitized mice, the IL-5 mRNA was expressed predominantly by CD34-positive (CD34+) progenitor cells. Following sensitization and allergen challenge, CD3-positive (CD3+) T lymphocytes were the major source of this cytokine. These results demonstrate the presence of IL-5 within the bone marrow of normal Balb/c mice. After sensitization and allergen challenge, the increase in IL-5-producing cells within the bone marrow is attributed by T lymphocytes.
authors.affiliation: Meakins-Christie Laboratories and Montreal Chest Institute Research Center, McGill University, Montreal, Canada.
authors.forename: E M
authors.initials: EM
authors.lastname: Minshall
authors.forename: R
authors.initials: R
authors.lastname: Schleimer
authors.forename: L
authors.initials: L
authors.lastname: Cameron
authors.forename: M
authors.initials: M
authors.lastname: Minnicozzi
authors.forename: R W
authors.initials: RW
authors.lastname: Egan
authors.forename: J C
authors.initials: JC
authors.lastname: Gutierrez-Ramos
authors.forename: D H
authors.initials: DH
authors.lastname: Eidelman
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
mesh_terms: D000485:Allergens / Q000009:adverse effects*; D000818:Animals; D018952:Antigens, CD34 / Q000032:analysis; D001249:Asthma / Q000276:immunology / Q000473:pathology; D001798:Blood Proteins / Q000032:analysis; D001853:Bone Marrow / Q000276:immunology*; D017252:CD3 Complex / Q000032:analysis; D002454:Cell Differentiation; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000276:immunology / Q000502:physiology; D005786:Gene Expression Regulation; D006412:Hematopoietic Stem Cells / Q000276:immunology / Q000473:pathology; D007114:Immunization; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D018836:Inflammation Mediators / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis* / Q000235:genetics; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000009:adverse effects; D010641:Phenotype; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D012260:Ribonucleases; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
chemical_list: D000485:Allergens; D018952:Antigens, CD34; D001798:Blood Proteins; D017252:CD3 Complex; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D015848:Interleukin-5; D012333:RNA, Messenger; D010047:Ovalbumin; D012260:Ribonucleases