학술논문

Role of interleukin-18 and T-helper type 1 cytokines in the development of Mycoplasma pneumoniae pneumonia in adults.
Document Type
Journal Article
Source
CHEST. May2002, Vol. 121 Issue 5, p1493-1497. 5p.
Subject
*MYCOPLASMA pneumoniae infections
*INTERLEUKINS
*CYTOKINES
*PNEUMONIA in children
Language
ISSN
0012-3692
Abstract
Study Objective: Interleukin (IL)-18 is a proinflammatory cytokine, originally termed interferon (IFN)-gamma-inducing factor, which promotes T-helper type 1 (Th1) cytokine responses. We recently reported that serum IL-18 levels were elevated in children with Mycoplasma pneumoniae pneumonia (MP). In this study, we investigated the contribution of IL-18 to the infection and assessed the Th1 cytokine response to pulmonary involvement in adults.Methods: We investigated the clinical course, pulmonary involvement, and serum levels of IL-18, IFN-gamma, IL-12p40, and soluble IL-2 receptor (sIL-2R) in 21 patients with acute-stage MP and in 21 age- and sex-matched control subjects.Results: Significantly (p < 0.001) increased serum IL-18 (median, 248 pg/mL [range, 89 to 441 pg/mL] vs. median, 126 pg/mL [range, 47 to 217 pg/mL]) and sIL-2R (median, 617 U/mL [range, 410 to 1,032 U/mL] vs. median, 425 U/mL [range, 268 to 601 U/mL]) were found in patients with MP as compared with healthy control subjects, and there was a tendency toward increased serum IFN-gamma and IL-12p40. Circulating IL-18 values had a positive correlation with serum sIL-2R levels (r = 0.62, p = 0.028) and the number of affected pulmonary lobes (sigma = 0.61, p = 0.024), but not with the serum levels of antibodies to M pneumoniae, IFN-gamma, or IL-12p40. Serum IL-18 and sIL-2R values in severe cases were significantly higher (p < 0.03) than those in mild cases. IFN-gamma and sIL-2R levels in four patients with pleural effusion were significantly (p < 0.05) higher than those in the other 17 subjects.Conclusions: Serum levels of IL-18 were raised during the acute phase of MP. We suggest IL-18 and Th1 cytokines may play a significant role in the immunopathologic responses in MP. [ABSTRACT FROM AUTHOR]