ABSTRACT
Aggregatibacter actinomycetemcomitans, an etiological agent associated with periodontitis, endocarditis, and other infections, has rarely been implicated in spondylitis. A 70-year-old man with aortic valve replacement presented with a 4-month history of lower back pain and was diagnosed with spondylitis. Prolonged incubation of blood cultures and a biopsy yielded A. actinomycetemcomitans. Concurrent infective endocarditis (IE) was probable considering the infectious organism and the patients' prosthetic valve. The patient was treated with ceftriaxone and recovered well. Pyogenic spondylitis with possible concurrent IE may be caused by A. actinomycetemcomitans. Extended incubation and repeated cultures should be considered if Haemophilus spp., Aggregatibacter spp, Cardiobacterium spp, Eikenella spp, and Kingella spp. (HACEK) infection is suspected.
Subject(s)
Cardiobacterium , Endocarditis, Bacterial , Spondylitis , Aged , Aggregatibacter actinomycetemcomitans , Anti-Bacterial Agents/therapeutic use , Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/drug therapy , Haemophilus , Humans , Male , Spondylitis/diagnosisABSTRACT
miR-1 and miR-133 are clustered on the same chromosomal loci and are transcribed together as a single transcript that is positively regulated by ecotropic virus integration site-1 (EVI1). Previously, we described how miR-133 has anti-tumorigenic potential through repression of EVI1 expression. It has also been reported that miR-1 is oncogenic in the case of acute myeloid leukemia (AML). Here, we show that expression of miR-1 and miR-133, which have distinct functions, is differentially regulated between AML cell lines. Interestingly, the expression of miR-1 and EVI1, which binds to the promoter of the miR-1/miR-133 cluster, is correlative. The expression levels of TDP-43, an RNA-binding protein that has been reported to increase the expression, but inhibits the activity, of miR-1, were not correlated with expression levels of miR-1 in AML cells. Taken together, our observations raise the possibility that the balance of polycistronic miRNAs is regulated post-transcriptionally in a hierarchical manner possibly involving EVI1, suggesting that the deregulation of this balance may play some role in AML cells with high EVI1 expression.
