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Published online before print January 10, 2007

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0706435

Received for publication July 6, 2006.
Revised December 8, 2006.
Accepted for publication December 8, 2006.

Article

Role of human neutrophil peptides in the initial interaction between lung epithelial cells and CD4⁺ lymphocytes

Departments of Anaesthesia, Critical Care Medicine and Physiology, Division of Respiratory Medicine, University of Toronto, St. Michael’s Hospital, Toronto, Ontario, Canada

^@ To whom correspondence should be addressed. E-mail: haibo.zhang{at}utoronto.ca.

	Abstract

Human neutrophil peptides (HNP) exert immune-modulating effects. We hypothesized that HNP link innate and adaptive immunity through activation of costimulatory molecules. Human lung epithelial cells and CD4⁺ lymphocytes were treated with HNP separately or in coculture. Stimulation with HNP induced an increase in cell surface expression of CD54 (ICAM-1), CD80, and CD86 on lung epithelial cells and the corresponding major ligands, CD11a (LFA-1), CD152 (CTLA-4), and CD28 on CD4⁺ lymphocytes. There was an increased nuclear expression of the transcription factor p53 in human alveolar A549 cells and an elevated NF-B (p50) and a degradation of I-B protein in CD4⁺ lymphocytes following HNP stimulation. HNP enhanced the interaction between A549 cells and CD4⁺ lymphocytes by increasing cell adhesion and release of IFN-, IL-2, and IL-8. This was attenuated by using an 1-proteinase inhibitor to neutralize HNP. We conclude that HNP play an important role in linking innate to acquired immunity by activation of costimulatory molecules in lung epithelial cells and CD4⁺ lymphocytes.

Key Words: infection • immunity • cytokine

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