Conversely, bacterial infection and LPS stimulation enhance expression of miR-15a and miR-16 in BMDM but myeloid-specific deletion of the locus encoding miR-15a/16 resulted in increased phagocytosis of FITC-labeled E. coli due to increased expression of the LPS receptor TLR-4 (40). Here, TLR4 is linked to bacterial infectious disease.