PT  - JOURNAL ARTICLE
AU  - J. Gabrijelcic
AU  - A. Acuña
AU  - M. Profita
AU  - A. Paternò
AU  - K.F. Chung
AU  - A.M. Vignola
AU  - R. Rodríguez-Roisin
TI  - Neutrophil airway influx by platelet-activating factor in asthma: role of adhesion molecules and LTB<sub>4</sub> expression
AID  - 10.1183/09031936.03.00098102
DP  - 2003 Aug 01
TA  - European Respiratory Journal
PG  - 290--297
VI  - 22
IP  - 2
4099  - http://erj.ersjournals.com/content/22/2/290.short
4100  - http://erj.ersjournals.com/content/22/2/290.full
SO  - Eur Respir J2003 Aug 01; 22
AB  - Platelet-activating factor (PAF)-induced neutrophil lung sequestration may require cell surface adhesion molecules (macrophage‐1 antigen (MAC‐1) and lymphocyte function-associated antigen‐1 (LFA‐1)). In this randomised, double-blinded, crossover study, theneutrophil kinetics after PAF and Lyso-PAF (L‐PAF) airway challenge were investigated in nine mild-intermittent asthmatics. Neutrophils were measured in peripheral blood (PB) before and at 5, 15, 45 and 240 min after bronchoprovocation, and in induced sputum before and at 240 min after challenge. MAC‐1 and LFA‐1 expression were assessed by immunocytochemistry, and leukotriene B4 (LTB4) was measured by enzyme-immunoassay in induced-sputum supernatants. Compared with baseline, neutrophils in PB decreased 5 min after PAF, while at 240 min neutrophils in induced sputum increased. Compared with baseline and L‐PAF, PAF decreased the percentages of MAC‐1‐ and LFA‐1‐positive neutrophils in PB at 5 min, but increased the percentages of MAC‐1 and LFA‐1 in neutrophil-induced sputum. Moreover, compared with baseline and L‐PAF, PAF-induced sputum revealed higher LTB4 levels, a finding that correlated with the elevated number of neutrophils in induced sputum. These findings suggest that macrophage‐1 antigen and lymphocyte function-associated antigen‐1 are involved in platelet-activating factor-induced neutrophil lung traffic, and that this process is modulated by enhanced leukotriene B4 release within the airways. This study was supported by the Comissionat per a Universitats i Recerca de la Generalitat de Catalunya (2001-SGR00386), a Research Grant (2000) from the European Respiratory Society (ERS), Ministerio de Sanidady Consumo (Redes Temátions de Investigación Cooperativa, CO3/11) and a grant-in-aid from Esteve Group. A. Acuña was supported byFundación Gran Mariscal de Ayacucho, Caracas, Venezuela, and Instituto de Cooperación Iberoamericana (ICI), Spain.