Myeloid PDLIM2 repression as a common causal mechanism of lung disease pathogenesis and susceptibility to infection

Selective deletion of PDLIM2 in myeloid cells rendered mice more vulnerable to lung injury and mortality after LPS intratracheal instillation, which was associated with the exacerbated activation of pro-inflammation signaling pathways and the more diminished activation of anti-inflammation signaling pathways in the lung, and particularly, in lung macrophages and neutrophils. Overall design: The experiments started with WT and Pdlim2 myeloid KO (mKO) mice of similar age. Each group was further divided into PBS and LPS-treated ones where treatment was administered through intratracheal injection. Lungs from these 4 groups of mice were dissected 48hr post treatment and were then dissociated into single cell suspension. scRNAseq was done with the combination of 10x genomics single cell 5' kit and customized sample multiplexing using TotalSeq CD45 tag antibody.