Literature DB >> 1735191

Levels of soluble IL-2 receptor in plasma from asthmatics. Correlations with blood eosinophilia, lung function, and corticosteroid therapy.

P Lassalle1, M Sergant, Y Delneste, P Gosset, B Wallaert, M Zandecki, A Capron, M Joseph, A B Tonnel.   

Abstract

Evidence now suggests that eosinophils and T lymphocytes infiltrating bronchial tissues may play a key role in the pathophysiology of asthma. Circulating eosinophils, lung function, and plasma soluble IL-2 receptor (sIL-2R) were measured in 42 asthmatic patients referred for symptomatic asthma. The patients were divided into two groups based on the presence or absence of atopy. The group of non-atopic asthmatics was further divided according to the patients' requirement for long term oral corticosteroids. The mean sIL-2R +/- s.d. was 36.3 +/- 9.9 pM in the control group, 28.9 +/- 9.2 pM in the atopic asthmatics, 43.3 +/- 18.07 pM in the non-atopic asthmatics without oral steroid therapy, but was increased in the steroid-treated group (62.2 +/- 19.3 pM, P less than 0.01). A significant correlation was found between FEV1 and circulating eosinophils in atopic asthmatics and in non-atopic asthmatics without oral corticosteroid therapy, but not in the steroid-treated group. Furthermore, significant correlations were found between sIL-2R and FEV1, and between sIL-2R and blood eosinophils, in the group of non-atopic asthmatics not on oral steroid therapy. No such correlations were evidenced in the other groups of asthmatics. Similar results were obtained during the clinical course of three non-atopic patients followed for more than 1 year. These data suggest that T cell activation appears more prominent in non-atopic asthma than in atopic asthma. Moreover, it appears that T cell activation can occur in severe forms of asthma despite steroid treatment. Finally, the results suggest a possible link between T cell activation, eosinophils, and lung function, which may reflect a particular pathogenetic mechanism involved in non-atopic asthma.

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Year:  1992        PMID: 1735191      PMCID: PMC1554276          DOI: 10.1111/j.1365-2249.1992.tb02986.x

Source DB:  PubMed          Journal:  Clin Exp Immunol        ISSN: 0009-9104            Impact factor:   4.330


  14 in total

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Authors:  M Azzawi; B Bradley; P K Jeffery; A J Frew; A J Wardlaw; G Knowles; B Assoufi; J V Collins; S Durham; A B Kay
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Authors:  K J Taylor; A R Luksza
Journal:  Thorax       Date:  1987-06       Impact factor: 9.139

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4.  Eosinophils, bronchial hyperreactivity and late-phase asthmatic reactions.

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Authors:  H J Horst; H D Flad
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6.  Eosinophilic inflammation in asthma.

Authors:  J Bousquet; P Chanez; J Y Lacoste; G Barnéon; N Ghavanian; I Enander; P Venge; S Ahlstedt; J Simony-Lafontaine; P Godard
Journal:  N Engl J Med       Date:  1990-10-11       Impact factor: 91.245

Review 7.  The soluble interleukin-2 receptor: biology, function, and clinical application.

Authors:  L A Rubin; D L Nelson
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8.  Total eosinophil counts in the management of bronchial asthma.

Authors:  B R Horn; E D Robin; J Theodore; A Van Kessel
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9.  Cellular events in the bronchi in mild asthma and after bronchial provocation.

Authors:  R Beasley; W R Roche; J A Roberts; S T Holgate
Journal:  Am Rev Respir Dis       Date:  1989-03

10.  CD4 T-lymphocyte activation in acute severe asthma. Relationship to disease severity and atopic status.

Authors:  C J Corrigan; A B Kay
Journal:  Am Rev Respir Dis       Date:  1990-04
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7.  Elevation of soluble interleukin-2 receptor levels in nasal allergy.

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  7 in total

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