Eosinophilia, interleukin‐5, and tumour necrosis factor‐alpha in asthmatic children

Hughes, JM; Rimmer, S. J.; Salome, Cheryl M.; Hodge, Linda; Liu-Brennan, Damien; Woolcock, A J; Armour, Carol

doi:10.1034/j.1398-9995.2001.056005412.x

Cited by 16 publications

(14 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, non-significant decrease was observed in serum IL-5 after 2 months of treatment with inhaled corticosteroids. This is in agreement with other reports [10,24] .They reported non-significant reduction of IL-5 after treatment with inhaled corticosteroids. However, this reported decrease of IL-5 may be related to the inhibitory role of inhaled corticosteroids as an anti-inflammatory drug on Th2 cells with subsequent suppression of IL-4 and IL-5 production [25].…”

Section: Discussionsupporting

confidence: 83%

Serum Interleukin-5 Changes in Partly Controlled Atopic Asthmatic Children

2014

Maced J Med Sci

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 83%

Serum Interleukin-5 Changes in Partly Controlled Atopic Asthmatic Children

2014

Maced J Med Sci

View full text Add to dashboard Cite

show abstract

“…To learn whether IL-5 stimulates static adhesion to the soluble VCAM-1 splice forms, EOS were incubated with IL-5 and studied in cell adhesion assays. EOS incubated with 50 pg/ml IL-5, a concentration within the physiological range measured in the serum of human asthmatics (42)(43)(44), exhibited an ϳ1.5-fold enhancement in maximum adhesion to both 6d-VCAM-1 ( Fig. 2A) and 7d-VCAM-1 ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The loop between ␤ strands C and D in the first immunoglobulin (Ig)-like module is accessible on the protein surface and contains the core integrin-recognition sequence Ile 39 -Asp-Ser-Pro-Leu 43 (IDSPL) (11)(12)(13)(14)(15). A second IDSPL site is present in the CD loop in module 4 (12,14).…”

mentioning

confidence: 99%

Differential Engagement of Modules 1 and 4 of Vascular Cell Adhesion Molecule-1 (CD106) by Integrins α4β1 (CD49d/29) and αMβ2 (CD11b/18) of Eosinophils

Barthel

Annis

Mosher

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

We have studied adhesion of eosinophils to various forms of vascular cell adhesion molecule 1 (VCAM-1, CD106), an integrin counter-receptor implicated in eosinophil recruitment to the airway in asthma. Full-length 7d-VCAM-1, with seven immunoglobulin-like modules, contains integrin-binding sites in modules 1 and 4. The alternatively spliced six-module protein, 6d-VCAM-1, lacks module 4. In static assays, unactivated purified human blood eosinophils adhered similarly to recombinant soluble human 6d-VCAM-1 and 7d-VCAM-1 coated onto polystyrene microtiter wells. Further experiments, however, revealed differences in recognition of modules 1 and 4. Antibody blocking indicated that eosinophil adhesion to 6d-VCAM-1 or a VCAM-1 construct containing only modules 1-3, 1-3VCAM-1, is mediated by ␣4␤1 (CD49d/29) ,whereas adhesion to a construct containing modules 4 -7, 4 -7VCAM-1, is mediated by both ␣4␤1 and ␣M␤2 (CD11b/18). Inhibitors of phosphoinositide 3-kinase, which block adhesion of eosinophils mediated by ␣M␤2, blocked adhesion to 4 -7VCAM-1 but had no effect on adhesion to 6d-VCAM-1. Consistent with the antibody and pharmacological blocking experiments, eosinophilic leukemic cell lines lacking ␣M␤2 did not adhere to 4 -7VCAM-1 but did adhere to 6d-VCAM-1 or 1-3VCAM-1. Activation of eosinophils by interleukin (IL)-5 enhanced static adhesion to 6d-VCAM-1, 7d-VCAM-1, or 4 -7VCAM-1; IL-5-enhanced adhesion to all 3 constructs was blocked by anti-␣M␤2. Adhesion of unstimulated eosinophils to 7d-VCAM-1 under flow conditions was inhibited by anti-␣4 or anti-␣M. IL-5 treatment decreased eosinophil adhesion to 7d-VCAM-1 under flow, and anti-␣M had the paradoxical effect of increasing adhesion. These results demonstrate that ␣M␤2 modulates ␣4␤1-mediated eosinophil adhesion to VCAM-1 under both static and flow conditions. Vascular cell adhesion molecule 1 (VCAM-1)2 is a multimodular cell-surface glycoprotein up-regulated on human endothelium in response to pro-inflammatory cytokines in the asthmatic lung (1) and has been implicated in recruitment of eosinophils (EOS) from blood to the airway in asthma (2). Heterodimeric integrin receptors interacting with VCAM-1 are important in the rolling, firm adhesion, and movement of EOS (3, 4). These events are regulated by cytokines, which may alter integrin adhesive activity (5, 6). EOS express at least three potential integrin receptors that may be involved in adhesion to VCAM-1: ␣4␤1 (7-9), ␣D␤2 (7), and ␣4␤7 (8 -11).Considerable information is available about features of human VCAM-1 that are important for adhesion. The loop between ␤ strands C and D in the first immunoglobulin (Ig)-like module is accessible on the protein surface and contains the core integrin-recognition sequence Ile 39 -Asp-Ser-Pro-Leu 43 (IDSPL) (11-15). A second IDSPL site is present in the CD loop in module 4 (12, 14). Based on topology of exons within the mammalian genome and the similarity in amino acid sequence, a three-module unit was likely duplicated to generate VCAM-1 modules 1-3 and 4 -6 (16, 17). Modul...

show abstract

“…A variety of studies [49][50][51][52][53][54][55][56][57] analyzed cytokine levels in body fluids [serum, sputum, BAL fluid (BALF) or all] from patients with asthma compared with healthy or disease-control individuals. The majority of these studies found that Th2-associated cytokines were elevated in body fluids from asthmatics compared with control individuals.…”

Section: Cytokines and Chemokinesmentioning

confidence: 99%