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Acinetobacter baumannii  ( A .  baumannii ) is a significant cause of severe nosocomial pneumonia in immunocompromised individuals world-wide. With limited treatment options available, a better understanding of host immnity to  A .  baumannii  infection is critical to devise alternative control strategies. Our previous study has identified that intracellular Nod1/Nod2 signaling pathway is required for the immune control of  A .  baumannii  in airway epithelial cells  in vitro . In the current study, using Nod2 −/−  mice and an  in vivo  sublethal model of pulmonary infection, we show that Nod2 contributes to the early lung defense against  A .  baumannii  infection through reactive oxygen species (ROS)/reactive nitrogen species (RNS) production as Nod2 −/−  mice showed significantly reduced production of ROS/RNS in the lungs following  A .  baumannii  infection. Consistent with the higher bacterial load,  A .  baumannii -induced neutrophil recruitment, cytokine/chemokine response and lung pathology was also exacerbated in Nod2 −/−  mice at early time points post-infection. Finally, we show that administration of Nod2 ligand muramyl dipeptide (MDP) prior to infection protected the wild- type mice from  A .  baumannii  pulmonary challenge. Collectively, Nod2 is an important player in the early lung immunity against  A .  baumannii  and modulating Nod2 pathway could be considered as a viable therapeutic strategy to control  A .  baumannii  pulmonary infection.

Nod2 is required for the early innate immune clearance of Acinetobacter baumannii from the lungs