Inflammation involves a coordinated, sequential, and self limiting sequence of events controlled by positive and negative regulatory mechanisms. Among these, recent studies have shown that microRNAs (miRNAs), an evolutionarily conserved class of endogenous 22-nucleotide noncoding RNAs, contribute to the regulation of inflammation by repressing gene expression at the posttranscriptional level. In this study, we characterize the profile of miRNAs induced by LPS in human polymorphonuclear neutrophils (PMN) and monocytes. In particular, we identify miR-9 as the only miRNA (among 365 analyzed) upregulated in both cell types after TLR4 activation. Additionally, miR-9 is induced also by TLR2 agonists and by the proinflammatory cytokines TNF- and IL-1but not by IFN. Among the three different genes encoding miR-9 precursors in humans, we show that LPS selectively induces the transcription of miR-9-1 located in the CROC4 locus, in a MyD88- and NF-B-dependent manner. Both in PMN and monocytes, LPS regulates NFKB1 both at the transcriptional and post-transcriptional levels, and a conserved miR-9 seed sustained a miR-9-dependent inhibition of the NFKB1 transcript. Overall, these data suggest that TLR4-activated NF-B rapidly increases the expression of miR-9 that operates a feed-back control of the NF-B-dependent responses by fine tuning the expression of a key member of the NF-B family.