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Reduced Interleukin-18 Levels in BAL Specimens From Patients With Asthma Compared to Patients With Sarcoidosis and Healthy Control Subjects^*

^* From the Osler Chest Unit (Dr. Ho), Churchill Hospital, Oxford; and The Respiratory Unit (Drs. Denison, Wood, and Greening, and Ms. Davis), Western General Hospital, Edinburgh, UK.

Correspondence to: Ling-Pei Ho, MD, Osler Chest Unit, Churchill Hospital, Oxford OX3 7LJ, United Kingdom; e-mail: Ling-Pei.Ho{at}imm.ox.ac.uk

Study objectives: To investigate whether differing airway interleukin (IL)-18 levels may be implicated in the pathogenesis of asthma and sarcoidosis.

Setting: University teaching hospital.

Patients and methods: IL-18 levels were measured in BAL fluid and in the supernatant of lipopolysaccharide (LPS)-stimulated alveolar macrophages obtained by BAL from 15 patients with sarcoidosis, 11 patients with asthma, and 13 healthy subjects. We also examined the relationship between IL-18 levels and macrophage and lymphocyte concentrations in BAL fluid. IL-18 was measured using an in-house enzyme-linked immunosorbent assay.

Results: IL-18 levels were significantly lower in BAL fluid from patients with asthma (median, 0.0 pg/mL; interquartile range, 0.0 to 0.0 pg/mL) compared to patients with sarcoidosis (median, 222.0 pg/10⁶; interquartile range, 110 to 340 pg/mL; p = 0.009, Mann Whitney rank-sum test) and healthy control subjects (median, 162 pg/mL; interquartile range, 38 to 203 pg/mL; p = 0.025, Mann Whitney rank-sum test). Individual analyses comparing IL-18 levels with BAL macrophage counts, and IL-18 with lymphocyte counts in the three groups showed no correlation between these indexes. The mean levels of IL-18 in unstimulated macrophage supernatants were 410 pg/10⁶ cells for patients with asthma, 723.4 pg/10⁶ cells for patients with sarcoidosis, and 734.8 pg/10⁶ cells for healthy control subjects (p > 0.05). Stimulated macrophages from patients with sarcoidosis responded with increasing amounts of IL-18 at lower doses of LPS than macrophages from healthy control subjects or patients with asthma.

Conclusion: Our findings suggest that inherently low levels of IL-18 may be associated with the pathogenesis of asthmatic airway inflammation.

Key Words: asthma • BAL • interleukin-18 • macrophage stimulation • sarcoidosis • T-helper type 1/T-helper type 2 lymphocytes

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