Alveolar recruitment of ficolin-3 in response to acute pulmonary inflammation in humans.

Background: Ficolins serve as soluble recognition molecules in the lectin pathway of complement. They are known to participate in the systemic host-response to infection but their role in local pulmonary defence is still incompletely understood. The purpose of this study was to clarify whether acute lung and systemic inflammation induce recruitment of lectins in humans.

Methods: Fifteen healthy volunteers received LPS intravenously (IV) or in a lung subsegment on two different occasions. Volunteers were evaluated by consecutive blood samples and by bronchoalveolar lavage 2, 4, 6, 8, or 24h after LPS (n=3 in all groups), and gene expression patterns and protein levels of mannose-binding lectin (MBL) and ficolins were determined.

Results: Endobronchial LPS was associated with an increase in alveolar ficolin-3 and MBL levels (p<0.04 and p<0.001, respectively). IV LPS elicited a pronounced acute phase response with an increase in CRP (p<0.001) and plasma ficolin-1 protein levels (p<0.001), whereas no changes were observed in ficolin-1 gene expression patterns (p=0.11) or plasma protein levels of MBL, ficolin-2, or ficolin-3.

Conclusions: LPS induces a tissue-specific recruitment of ficolin-3 and ficolin-1 in the lung and systemic compartment, respectively, suggesting an important role of distinct lectin complement pathway initiators in the local pulmonary and systemic host defence.