title: Beta 2-adrenoceptor stimulation augments the IL-4-induced CD23 expression and release and the expression of differentiation markers (CD14, CD18) by the human monocytic cell line, U 937.
abstract: The effect of beta 2-adrenoceptor agonists and interleukin-4 (IL-4) on the CD23 expression on, and release from, the human promonocytic cell line, U 937, was investigated. As assessed by flow cytometry, incubation of U 937 cells in the presence of salbutamol, fenoterol or IL-4 induced a concentration- and time-dependent increase in CD23 expression, that was maximal after 48 hr and followed by a decrease thereafter. In addition, salbutamol potentiated the effect of IL-4, the optimal concentration of the drug being a function of the concentration of this cytokine. This synergy between IL-4 and beta 2-adrenoceptor agonists was also observed for the release of the soluble form of CD23. The effect on CD23 expression of salbutamol and fenoterol, but not of IL-4, was blocked in the presence of D,L-propranolol (1 microM) or butoxamine (1 microM). The alpha-adrenoceptor agonist, norepinephrine (1 microM), was ineffective in inducing CD23 expression or potentiating the one evoked by IL-4. Salbutamol down-regulated the expression of Fc gamma RI (CD64) and Fc gamma RII (CD32) whereas IL-4 was ineffective. Only when added together at the onset of the culture did salbutamol and IL-4 induce, after 48 hr, the expression of the monocyte marker, CD14. The expression of CD18 was up-regulated in response to salbutamol either alone or in combination with IL-4, this cytokine alone being inefficient. These data suggest that IL-4 and beta 2-adrenoceptor agonists induce differentiation of U 937 cells into monocyte-like cells.
authors.affiliation: Laboratoire d'Immuno-allergologie, Institut Henri Beaufour, Les Ulis, France.
authors.forename: N
authors.initials: N
authors.lastname: Paul-Eugene
authors.forename: B
authors.initials: B
authors.lastname: Dugas
authors.forename: J
authors.initials: J
authors.lastname: Gordon
authors.forename: J P
authors.initials: JP
authors.lastname: Kolb
authors.forename: J A
authors.initials: JA
authors.lastname: Cairns
authors.forename: M
authors.initials: M
authors.lastname: Paubert-Braquet
authors.forename: J M
authors.initials: JM
authors.lastname: Mencia-Huerta
authors.forename: P
authors.initials: P
authors.lastname: Braquet
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000420:Albuterol / Q000494:pharmacology; D015703:Antigens, CD / Q000096:biosynthesis*; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis*; D002078:Butoxamine / Q000494:pharmacology; D018821:CD18 Antigens; D002454:Cell Differentiation / Q000187:drug effects; D002772:Cholera Toxin / Q000494:pharmacology; D000242:Cyclic AMP / Q000096:biosynthesis; D004357:Drug Synergism; D005280:Fenoterol / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects*; D006412:Hematopoietic Stem Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D015847:Interleukin-4 / Q000494:pharmacology*; D018950:Lipopolysaccharide Receptors; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D017455:Receptors, IgE / Q000096:biosynthesis*; D017452:Receptors, IgG / Q000096:biosynthesis; D011994:Recombinant Proteins / Q000494:pharmacology; D015290:Second Messenger Systems; D014407:Tumor Cells, Cultured
chemical_list: D000318:Adrenergic beta-Agonists; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018821:CD18 Antigens; D018950:Lipopolysaccharide Receptors; D011943:Receptors, Adrenergic, beta; D017455:Receptors, IgE; D017452:Receptors, IgG; D011994:Recombinant Proteins; D002078:Butoxamine; D015847:Interleukin-4; D005280:Fenoterol; D002772:Cholera Toxin; D011433:Propranolol; D000242:Cyclic AMP; D000420:Albuterol; D009638:Norepinephrine