title: Decreased IL-15 may contribute to elevated IgE and acute inflammation in atopic dermatitis.
abstract: PBMC and acute skin lesions of patients with atopic dermatitis (AD) are characterized by increased IL-4 and IL-13, but decreased IFN-gamma production. This bias toward an increased Th2 cytokine profile may contribute to the elevated IgE levels and acute skin inflammation seen in AD. In this study, we examined the levels of IL-15, a Th1-like cytokine, in the PBMC and the skin lesions of AD patients. IL-15 secretion by Staphylococcal enterotoxin B-treated PBMC of AD patients was significantly lower than that of normals and psoriasis patients (p < 0.001). Membrane-bound IL-15 expression as measured by mean fluorescence intensity and percentage of IL-15-positive cells in Staphylococcal enterotoxin B-treated monocytes of AD patients (644 +/- 49% and 12.7 +/- 0.6%, respectively) were significantly lower than that of normals (869 +/- 56% and 15.8 +/- 1.2%, respectively) and psoriasis patients (1488 +/- 217% and 22.7 +/- 0.8%, respectively; p < 0.0007 and p < 0.0001, respectively). The membrane-bound IL-15 expression was also significantly lower in the control monocytes of AD patients compared with that in normals and psoriasis patients. There was no significant difference in the absolute number or percentage of monocytes between the study subjects. However, psoriasis skin lesions were found to have significantly more IL-15 mRNA-expressing cells (22.4 +/- 1.7) compared with that in acute AD (7.5 +/- 1.7) and chronic AD (13.7 +/- 1.7) skin lesions (p < 0.05). IL-15 enhanced IFN-gamma production by the PBMC of AD patients (p < 0.01), but not by that of normal individuals or psoriasis patients. In addition, IL-15 was found to suppress IgE synthesis (p < 0.01) by the PBMC of AD patients. These data support the concept that reduced IL-15 expression may contribute to the pathogenesis of AD.
authors.affiliation: Division of Allergy and Immunology, Department of Pediatrics, The National Jewish Medical and Research Center, Denver, CO 80206, USA.
authors.forename: Peck Y
authors.initials: PY
authors.lastname: Ong
authors.forename: Qutayba A
authors.initials: QA
authors.lastname: Hamid
authors.forename: Jeffrey B
authors.initials: JB
authors.lastname: Travers
authors.forename: Ian
authors.initials: I
authors.lastname: Strickland
authors.forename: Muhamed
authors.initials: M
authors.lastname: Al Kerithy
authors.forename: Mark
authors.initials: M
authors.lastname: Boguniewicz
authors.forename: Donald Y M
authors.initials: DY
authors.lastname: Leung
mesh_terms: D000208:Acute Disease; D002478:Cells, Cultured; D002908:Chronic Disease; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D005434:Flow Cytometry; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007371:Interferon-gamma / Q000096:biosynthesis; D019409:Interleukin-15 / Q000235:genetics / Q000378:metabolism* / Q000502:physiology*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D009000:Monocytes / Q000276:immunology; D011565:Psoriasis / Q000276:immunology / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D012867:Skin / Q000276:immunology / Q000473:pathology
chemical_list: D019409:Interleukin-15; D012333:RNA, Messenger; D007073:Immunoglobulin E; D007371:Interferon-gamma