Intestinal carriage of methicillin-resistant Staphylococcus aureus in nasal MRSA carriers hospitalized in the neonatal intensive care unit

BACKGROUND: The current data regarding the correlation between the methicillin-resistant Staphylococcus aureus (MRSA) clones carried in the nasal cavity and digestive tract are inadequate. METHODS: MRSA strains were isolated from both the feces and nasal swabs of 21 nasal-MRSA carriers ranging from 10 to 104 days of age treated at the neonatal intensive care units of two hospitals. The molecular epidemiological characteristics of the isolates were determined: multilocus sequence types, spa-types, staphylococcal cassette chromosome mec (SCCmec) types, carriage of four exotoxin genes, and genes contained in commercially available kit. RESULTS: The feces of all nasal carriers contained MRSA at levels ranging from 4.0 × 10(2) to 2.8 × 10(8) colony forming units/g feces. The MRSA clones isolated from the feces and the nasal swabs of each patient were the same. Four MRSA clones, clonal complex (CC) 8-SCCmec IVl, CC8-SCCmec IVb, CC1-SCCmec IVa and CC5-SCCmec IIa were identified from 21 patients. All CC8-SCCmec IVl strains and one of three CC5-SCCmec IIa strains carried the toxic shock syndrome toxin gene. CONCLUSIONS: The feces of tested MRSA carriers contained the same MRSA clones as the nasal isolates in considerable amounts, suggesting that more careful attention should be paid for the handling of excrement in the case of newborn babies or infants than that of adults

Inhibition of HDAC and Signal Transduction Pathways Induces Tight Junctions and Promotes Differentiation in p63-Positive Salivary Duct Adenocarcinoma

Background: The p53 family p63 is essential for the proliferation and differentiation of various epithelial basal cells. It is overexpressed in several cancers, including salivary gland neoplasia. Histone deacetylases (HDACs) are thought to play a crucial role in carcinogenesis, and HDAC inhibitors downregulate p63 expression in cancers. Methods: In the present study, to investigate the roles and regulation of p63 in salivary duct adenocarcinoma (SDC), human SDC cell line A253 was transfected with siRNA-p63 or treated with the HDAC inhibitors trichostatin A (TSA) and quisinostat (JNJ-26481585). Results: In a DNA array, the knockdown of p63 markedly induced mRNAs of the tight junction (TJ) proteins cingulin (CGN) and zonula occuludin-3 (ZO-3). The knockdown of p63 resulted in the recruitment of the TJ proteins, the angulin-1/lipolysis-stimulated lipoprotein receptor (LSR), occludin (OCLN), CGN, and ZO-3 at the membranes, preventing cell proliferation, and leading to increased cell metabolism. Treatment with HDAC inhibitors downregulated the expression of p63, induced TJ structures, recruited the TJ proteins, increased the epithelial barrier function, and prevented cell proliferation and migration. Conclusions: p63 is not only a diagnostic marker of salivary gland neoplasia, but it also promotes the malignancy. Inhibition of HDAC and signal transduction pathways is, therefore, useful in therapy for p63-positive SDC cells