Related Experiment Videos
Airway epithelium expresses interleukin-18
L A Cameron1, R A Taha, A Tsicopoulos
1Meakins-Christie Laboratories and Montreal Chest Institute Research Center, McGill University, Quebec, Canada.
The European Respiratory Journal
|October 30, 1999
Summary
Interleukin-18 (IL-18) is expressed in the airway epithelium and its levels change with T-helper 1 and T-helper 2 immune responses, impacting inflammatory conditions like asthma and sarcoidosis.
Area of Science:
- Immunology
- Respiratory Medicine
- Cytokine Biology
Background:
- Interleukin-18 (IL-18) is a cytokine involved in inflammatory responses.
- Its role in pulmonary inflammation, particularly concerning T-helper (Th)1 and Th2 responses, requires further investigation.
Purpose of the Study:
- To investigate the pulmonary expression of IL-18 in the context of Th1 and Th2 immune responses.
- To examine IL-18 regulation in mouse models of LPS and ovalbumin (OVA) challenge and in human sarcoidosis and asthma.
Main Methods:
- In situ hybridization and immunocytochemistry were employed to quantify cells expressing IL-18, IFN-gamma, IL-5, and MBP in mouse lung tissue and human bronchial biopsies.
- Analysis included control groups, LPS-treated mice (Th1 model), OVA-challenged mice (Th2 model), and patients with sarcoidosis and asthma.
Main Results:
- IL-18 was localized to airway epithelium and mononuclear cells, with constitutive expression in normal lungs and controls.
- LPS challenge increased IL-18 mRNA and IFN-gamma positive cells, indicative of a Th1 response.
- OVA challenge showed decreased IL-18 mRNA positive cells but increased IL-5 and MBP positive cells, characteristic of a Th2 response.
- Human studies revealed increased IL-18 in sarcoidosis and decreased IL-18 in asthma tissues compared to controls.
Conclusions:
- Interleukin-18 is expressed in the airway epithelium.
- Pulmonary IL-18 expression is regulated by both Th1 and Th2 immune responses.
- These findings highlight IL-18's role in airway inflammation and its differential regulation in conditions like sarcoidosis and asthma.