Depletion of alveolar macrophages in CD11c diphtheria toxin receptor mice produces an inflammatory response

摘要: Alveolar macrophages play a critical role in initiating the immune response to inhaled pathogens and have been shown be first cell type infected following intranasal inoculation with several pathogens, including Francisella tularensis. In an attempt further dissect of alveolar Francisella, we selectively depleted using CD11c.DOG mice. mice express diphtheria toxin receptor (DTR) under control full CD11c promoter. Because do not DTR, tissue restricted expression primate DTR followed by treatment (DT) has widely used as tool immunology examine effect acute depletion specific subset normal development. We successfully via administration DT. However, macrophage was accompanied many other changes cellular composition cytokine/chemokine milieu lung that potentially impact innate adaptive responses. Importantly, observed transient influx neutrophils spleen. Our experience serves cautionary note researchers given complex occur DT must taken into account when analyzing data.