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Increased interleukin-13 expression in patients with sarcoidosis
H-P Hauber1, D Gholami, A Meyer
1Department of Internal Medicine, University Hospital Eppendorf, Hamburg, Germany. hans-peter.hauber@mcgill.ca
Thorax
|May 31, 2003
Summary
Interleukin 13 (IL-13) is increased in sarcoidosis patients, suggesting an anti-inflammatory role. This cytokine, found in bronchoalveolar lavage cells, may suppress tumour necrosis factor alpha (TNFalpha).
Area of Science:
- Immunology
- Respiratory Medicine
Background:
- Sarcoidosis is a systemic granulomatous disease of unknown etiology.
- Inflammation in sarcoidosis involves Th1 cytokines like tumor necrosis factor alpha (TNFalpha).
- Interleukin 13 (IL-13), a Th2 cytokine, can suppress TNFalpha in monocytes.
Purpose of the Study:
- To investigate the role of IL-13 as a potential anti-inflammatory cytokine in sarcoidosis.
- To assess IL-13 expression in patients with sarcoidosis compared to healthy controls.
Main Methods:
- RT-PCR was used to measure mRNA expression of IL-13, IL-4, IL-10, and TNFalpha in bronchoalveolar lavage (BAL) cells and peripheral blood mononuclear cells (PBM).
- IL-13 protein levels were quantified in BAL cell culture supernatants.
- Immunocytochemistry was performed to localize IL-13 protein in BAL cells.
- TNFalpha concentrations were measured with and without stimulation by recombinant human (rh) IL-13, rhIL-10, and lipopolysaccharide (LPS).
Main Results:
- IL-13 mRNA expression was significantly elevated in BAL cells and PBM of sarcoidosis patients compared to controls.
- TNFalpha mRNA expression was significantly higher in BAL cells of patients.
- IL-13 protein was detected in alveolar macrophages of patients and led to decreased TNFalpha concentrations.
- No significant differences in IL-4 or IL-10 mRNA expression were observed between groups.
Conclusions:
- IL-13 expression and secretion are increased in BAL cells and PBM in sarcoidosis.
- Alveolar macrophages are a potential source of IL-13 in sarcoidosis.
- IL-13 exhibits an anti-inflammatory effect by modulating TNFalpha in sarcoidosis.