Insufficient serum L-ficolin is associated with the disease progression in pulmonary Mycobacterium avium complex disease

<b>Backgrounds:</b> Nontuberculous mycobacteria infectious diseases are increasing worldwide. Pulmonary <i>Mycobacterium avium</i> complex (MAC) disease is difficult to treat with chemotherapy and is unknown as a mechanism of infection, infection route, disease onset, and severity. Ficolins are oligometric defense lectins. L-ficolin plays an important role in innate immunity. The aim of this study is to identify the roles of L-ficolin in pulmonary MAC disease patients. <b>Methods:</b> 61 Japanese patients with pulmonary MAC disease who were consulted at our hospital from April 2011 to September 2017 and control group consisted of 30 healthy subjects without respiratory disease were enrolled. The relationship between serum L-ficolin levels and the disease severity were assessed and anti-bacterial roles of L-ficolin were examined. <b>Results:</b> Serum L-ficolin was significantly lower in pulmonary MAC disease patients than in healthy subjects (1.69±1.27 μg/mL vs 3.96±1.42 μg/mL : p&lt;0.001). The cut off value based on the ROC analysis result was 2.38 μg/mL (AUC 0.90, sensitivity 83.6% and specificity 86.7%). Serum L-ficolin was significantly lower in the nodular bronchiectatic type than in the fibrocavitary type, and tended to be lower in the HRCT scoring high score group. <i>In vitro,</i> purified L-ficolin bound to <i>M.avium</i> and its cell wall major component lipoarabinomannan in a concentration dependent manner. In addition, recombinant L-ficolin suppressed the growth of <i>M.avium</i> in the medium in a concentration dependent manner. <b>Conclusions:</b> Insuffient serum L-ficolin is associated with the disease progression in pulmonary MAC disease and serum level of L-ficolin is a possible biomarker.