Transient ablation of alveolar macrophages leads to massive pathology of influenza infection without affecting cellular adaptive immunity

摘要: Alveolar macrophages (AMs), localized at the pulmonary air-tissue interface, are one of first lines defense that interact with inhaled airborne pathogens such as influenza viruses. By using a new CD169-DTR transgenic mouse strain we demonstrate specific and highly controlled in vivo ablation this myeloid cell subset leads to severe impairment innate, but not adaptive, immune responses critically affects progression disease. In fact, AM-ablated mice, infected normally sublethal dose PR8 virus, showed dramatically increased virus load lungs, airway inflammation, edema vascular leakage, which caused death animals. Our data highlight possibilities for therapeutic strategies focusing on modulation AMs, may efficiently boost innate infections.