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Early Pulmonary and Systemic Inflammation Leads to Tissue‐Specific Recruitment of Lectin Complement Pathway Initiators
Author(s) -
Plovsing Ronni,
Berg Ronan,
MuntheFog Lea,
Konge Lars,
Iversen Martin,
Møller Kirsten,
Garred Peter
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.972.7
Subject(s) - ficolin , mannan binding lectin , lectin pathway , lectin , complement system , lipopolysaccharide , inflammation , systemic inflammation , bronchoalveolar lavage , lung , immunology , collectin , medicine , alternative complement pathway , antibody , innate immune system , immune system
Objective We wanted to clarify whether lipopolysaccharide (LPS)‐induced pulmonary and systemic inflammation induces localized and systemic recruitment of mannose‐binding lectin (MBL) and ficolins. Methods We performed a randomized, double‐blind, placebo‐controlled, cross‐over study in 15 healthy volunteers that received Escherichia coli endotoxin (LPS, 4 ng/kg) intravenously (IV) or in a lung subsegment on two different occasions. Groups were evaluated by blood samples and by bronchoalveolar lavage 2, 4, 6, 8, or 24 hours post‐challenge; gene expression patterns and protein levels of MBL and ficolins were determined in both blood and lung. Results Endobronchial challenge with LPS was associated with an increase in alveolar ficolin‐3 levels, with a peak after 24 hours (p < 0.04),and an increase in alveolar MBL (p < 0.001). IV LPS challenge led to an increase in plasma ficolin‐1 protein levels (p < 0.001),whereas no changes were observed in ficolin‐1 gene expression patterns or plasma protein levels of MBL, ficolin‐2, or ficolin‐3. Conclusions LPS induces a tissue‐specific recruitment of ficolin‐3, MBL, and ficolin‐1 in the lung and circulation, suggesting an important role of lectin complement pathway initiators in both local and systemic host defense.