Effects of ClpP protease on biofilm formation of Enterococcus faecalis.

OBJECTIVES: Enterococcus faecalis (E. faecalis), one of the main pathogens responsible for refractory periapical periodontitis and nosocomial infections, exhibits markedly higher pathogenicity in biofilms. Studies have shown that caseinolytic protease P (ClpP) is involved in biofilm formation. However, to date, few studies have investigated the role of ClpP in the survival of E. faecalis, and in enhancing biofilm formation. Therefore, we investigated the role of ClpP in the formation of E. faecalis biofilms. METHODOLOGY: In our study, we used homologous recombination to construct clpP deleted and clpP complement strains of E. faecalis ATCC 29212. A viable colony counting method was used to analyze the growth patterns of E. faecalis. Crystal violet staining (CV) and confocal scanning laser microscopy (CLSM) were used to characterize biofilm mass formation and scanning electron microscopy (SEM) was used to observe the biofilm microstructure. Data was statistically analyzed via Student's t-test or one-way analysis of variance (ANOVA). RESULTS: The results exhibited altered growth patterns for the clpP deletion strains and depleted polysaccharide matrix, resulting in reduced biofilm formation capacity compared to the standard strains. Moreover, ClpP was observed to increase biofilm formation in E. faecalis. CONCLUSION: Our study shows that ClpP can increase biofilm formation in E. faecalis and emphasizes the importance of ClpP as a potential target against E. faecalis.

Mechanism of dexamethasone in the context of Toxoplasma gondii infection.

Toxoplasmosis is a serious zoonoses disease and opportunistic, and can be life-threatening. Dexamethasone (DEX) is widely used in the clinic for treatment of inflammatory and autoimmune diseases. However, long-term use of DEX is often easy to lead to acute toxoplasmosis in patients, and the potential molecular mechanism is still not very clear. The aims of this study were to investigate the effect of DEX on proliferation of Toxoplasma and its molecular mechanisms, and to establish the corresponding control measures. All the results showed that dexamethasone could enhance the proliferation of Toxoplasma gondii tachyzoites. After 72 h of DEX treatment, 566 (±7) tachyzoites were found in 100 host cells, while only 86 (±8) tachyzoites were counted from the non-treated control cells (P < 0·01). Gas chromatography (GC) analysis showed changes in level and composition of fatty acids in DEX-treated host cells, and T. gondii. Fish oil was added as a modulator of lipid metabolism in experimental mice. It was found that mice fed with fish oil did not develop the disease after infection with T. gondii, and the structure of fatty acids in plasma changed significantly. The metabolism of fatty acid in the parasites was limited, and the desaturase gene expression was downregulated. These results indicate that the molecular mechanism of dexamethasone to promote the proliferation of T. gondii may be that dexamethasone induces the change of fatty acids composition of tachyzoites and host cells. Therefore, we recommend supplementation of fatty acid in immunosuppressive and immunocompromised patients in order to inhibit toxoplasmosis.

Papillary breast lesions diagnosed by core biopsy require complete excision.

BACKGROUND: Surgical excision of papillary breast lesions with atypia diagnosed using core needle biopsy (CNB) has been accepted; however, the management of benign papillary lesions (without atypia) has been controversial. The purpose of this study was to evaluate the surgical outcome of nonmalignant papillary lesions diagnosed by ultrasound-guided 14-gauge CNB, and to establish clear guidelines on management of these lesions. METHODS: We retrospectively identified 268 nonmalignant papillary breast lesions, including 203 benign lesions and 65 atypical lesions, diagnosed by CNB and subsequently surgically excised in 250 women at our institution between July 2004 and October 2010. For each lesion, medical records and radiologic and pathologic reports were reviewed and coded. We compared the histological upgrade among the collected variables. RESULTS: On histological examination after surgical excision, 15.4% atypical papillary lesions and 5.9% benign lesions were upgraded to malignant, and 20.2% benign lesions were upgraded to atypical. Atypia (P = 0.015) was significantly associated with malignant upgrade at excision. No clinical or radiologic variable was helpful in predicting the possibility of histological upgrade of CNB-diagnosed nonmalignant papillary lesions. CONCLUSIONS: Nonmalignant papillary lesions diagnosed with CNB showed an unacceptable pathological upgrade rate after excision. Therefore, surgical excision should be performed for all papillary lesions of the breast for definitive diagnosis.