- Paper Report
- Open Access
Eosinophil recruitment in TNF-receptor-deficient mice
- Malcolm Shepherd1
© Biomed Central Ltd 2001
- Received: 4 June 2001
- Published: 14 September 2001
- Eosinophil recruitment, knockout mice, TNF receptor
Tumour necrosis factor (TNF) is increased in the airways of asthmatic patients; however, its contribution to allergic inflammation is unclear. Two different receptors (p55 and p75) in the mouse mediate different inflammatory responses to TNF-a. In this study TNF receptor gene knockout mice were used to investigate the role of TNF in allergic inflammation.
Mice deficient in P55 or P55/75 demonstrated significantly reduced, though not abolished, alveolar eosinophilia in response to airway challenge with ovalbumin. This was despite allergic sensitisation demonstrated by immediate skin test hypersensitivity. In conjunction, studies measuring eosinophil adhesion and rolling on mesenteric venules showed significant reduction in eosinophil trafficking in p55-deficient mice. In contrast, bronchial hypersensitivity to metacholine was preserved, possibly reflecting the persistent, though reduced, alveolar eosinophilia.
Gene knockout, BAL, airway resistance measurement, immunohistochemistry, eosinophil adhesion studies