Our work focuses on the early innate immune response to PTB infection. More specifically, this project focuses on the early interactions between tissue resident AM and other cell types such as lung epithelial cells (EC), recruited myeloid and lymphoid cells. Furthermore we aim to determine how these cellular interactions and the physical localization of AMs determines their effector functions during pulmonary Mtb infection. 
We developed a novel technique for labeling immune cells present in the airway or the vasculature using fluorophore conjugated antibodies administered by intratracheal (i.t.) instillation and intravenous injection (i.v.) prior to harvest, allowing us to determine not only the number and percentage of specific cell types by flow cytometry, but also their specific location in the lung at the time of harvest. Using this cutting edge technique, we demonstrated for the first time that during pulmonary Mtb infection with a hypervirulent clinical isolate of Mtb, AMs have the ability to egress from the airway to the interstitial and parenchymal lung tissue over time, guided by the CCR2-CCL2 axis, and that they have the ability to localize within TB granulomas in a CCR2 dependent manner (Dunlap et al. 2018). From there we found that airway and non-airway AMs have distinct transcriptional profiles marking different effector functions, where non-airway AMs have a marked increase in M1 profile associated genes involved in phagocytosis, complement interactions, iNOS mediated killing, MHCII driven antigen presentation and T cell interactions. These data demonstrated for the first time that tissue resident AMs have the ability to migrate during Mtb infection and have compartmentally distinct functional roles.