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Suppressed pulmonary expression of leptin in lipopolysaccharide‐induced acute and chronic lung inflammation
Author(s) -
Vernooy Juanita,
Cloots Roy,
Dentener Mieke,
Wouters Emiel
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a210-a
Subject(s) - leptin , inflammation , neutrophilia , medicine , lipopolysaccharide , lung , endocrinology , obesity
Leptin, originally described as an adipocyte‐derived hormone regulating energy expenditure, is now classified as a type I cytokine. We and others recently found that the lung is an additional source of leptin. The aim of the present study was to investigate the effect of acute and chronic inflammation on pulmonary expression of leptin. Methods Male Swiss mice were exposed intratracheally (IT) to 5 μg LPS ( E.coli O55:B5), whereas control mice received saline. Acute lung inflammation was induced by a single LPS dose and mice were killed 4h, 24h and 72h postexposure. Chronic lung inflammation was induced by repeated LPS exposure (twice a week for 12 weeks) and mice were killed after a 1‐wk or 8‐wks recovery period. Lungs were removed to assess cellular influx, leptin protein (immunohistochemistry) and mRNA (PCR). Results Acute LPS exposure induced a transient neutrophilia, whereas chronic LPS exposure resulted in persistent accumulation of macrophages and CD8+ T‐cells. Control mice displayed positive leptin staining in bronchiolar epithelium and alveolar macrophages. Both acute (4h, 24h, 72h) and chronic (1‐wk) inflammation was associated with complete suppression of pulmonary leptin expression at protein and mRNA level. Leptin expression was fully restored after the 8‐wk recovery period. Conclusion Lungs of mice display constitutive leptin expression in bronchiolar epithelium and alveolar macrophages. Acute and chronic lung inflammation results in complete suppression of pulmonary leptin expression. Our data suggest that downregulation of leptin expression in lung may contribute to the ongoing pulmonary inflammation.