Pulmonary collectins provide a first line of defense against L. Pneumophila through inhibiting their type IV secretion system

Background:; We have previously demonstrated that pulmonary collectins (SP-A and SP-D) attenuate intracellular growth of Legionella pneumophila. However, the molecular mechanisms have not been completely understood. To clarify the molecular mechanisms involved in inhibitory effect of pulmonary collectins. Methods: Using adenylate cyclase-reporter assay system, we quantitatively evaluated the activity of Type IV secretion system (TIVSS). Furthermore, we examined autophagic activity in THP-1 cells infected with L. pneumophila. Induction of autophagy was evaluated by western blotting using anti-LC3 and anti-p62 antibodies. Results: Pulmonary collectins inhibited secretion of effector molecules through TIVSS. Interaction between collectins and L. pneumophila seemed to be responsible for inhibitory effect. It has been reported that effector molecules secreted from L. pneumophila cause the delay in induction of autophagy. Consistent with the results in above, pulmonary collectins accelerated the induction of autophagy in L. pneumophila-infected cells. Conclusions: Delay of autophagy is crucial for intracellular growth of L. pneumophila. Our data suggest that pulmonary collectins attenuate the activity of TIVSS, and thereby accelerate induction of autophagy. Results in the present study clarify one of the molecular mechanisms by which pulmonary collectins inhibit intracellular growth of L. pneumophila.