HOME HELP FEEDBACK ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Permissions Request Permissions Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pilette, C. Articles by Sibille, Y. Search for Related Content PubMed Articles by Pilette, C. Articles by Sibille, Y.

Dual effect of neutrophils on secretory component production by human bronchial epithelial cells

Unit of Pneumology and Microbiology, University of Louvain (UCL), Brussels, Belgium

CORRESPONDENCE: Charles Pilette, Unit and Dept of Pneumology, University of Louvain (UCL), Brussels, Belgium

A decreased bronchial expression of secretory component (SC) was demonstrated in severe COPD, and correlated with neutrophils. Mechanisms of epithelial cell/neutrophils interactions remain however poorly understood.

Calu-3 (human bronchial epithelial) cells were incubated after confluence (in triplicate conditions) with various ratios of activated neutrophils (0.5:1 to 15:1, neutrophils: Calu-3 cells). After 48hrs of co-culture supernatants were assayed for SC by ELISA.

SC production by Calu-3 cells increased at intermediate neutrophil numbers (316±32 versus 193±19ng·ml^–1, ratio of 5:1 versus control, mean±SEM of 3 experiments, p = 0.05). In contrast, a trend for decrease in SC was observed with high neutrophil numbers (111±19 versus 193±19ng·ml^–1, ratio of 15:1 versus control, p = 0.06). The addition of secretory leukocyte protease inhibitor further increased SC upregulation at intermediate ratios, and inhibited the SC decrease at high neutrophil numbers. The mechanism of SC up-regulation by neutrophils did not implicate TNF- or IL-1ß.

This study provides direct evidence of a dual effect of neutrophils on epithelial SC. Our data suggest that neutrophils could differently affect epithelial immune secretory function according to the extent of neutrophil influx and/or to the reactivity of airway epithelial cells.