It's a trap! The development of a versatile drain biofilm model and its susceptibility to disinfection.

BACKGROUND: Pathogens in drain biofilms pose a significant risk for hospital-acquired infection. However, the evidence of product effectiveness in controlling drain biofilm and pathogen dissemination are scarce. A novel in-vitro biofilm model was developed to address the need for a robust, reproduceable and simple testing methodology for disinfection efficacy against a complex drain biofilm. METHODS: Identical complex drain biofilms were established simultaneously over 8 days, mimicking a sink trap. Reproducibility of their composition was confirmed by next-generation sequencing. The efficacy of sodium hypochlorite 1000 ppm (NaOCl), sodium dichloroisocyanurate 1000 ppm (NaDCC), non-ionic surfactant (NIS) and peracetic acid 4000 ppm (PAA) was explored, simulating normal sink usage conditions. Bacterial viability and recovery following a series of 15-min treatments were measured in three distinct parts of the drain. RESULTS: The drain biofilm consisted of 119 mixed species of Gram-positive and -negative bacteria. NaOCl produced a >4 log10 reduction in viability in the drain front section alone, while PAA achieved a >4 log10 reduction in viability in all of the drain sections following three 15-min doses and prevented biofilm regrowth for >4 days. NIS and NaDCC failed to control the biofilm in any drain sections. CONCLUSIONS: Drains are one source of microbial pathogens in healthcare settings. Microbial biofilms are notoriously difficult to eradicate with conventional chemical biocidal products. The development of this reproducible in-vitro drain biofilm model enabled understanding of the impact of biocidal products on biofilm spatial composition and viability in different parts of the drain.

Hematopoietic miR155 deficiency enhances atherosclerosis and decreases plaque stability in hyperlipidemic mice.

microRNA-155 (miR155) is a central regulator of immune responses that is induced by inflammatory mediators. Although miR155 is considered to be a pro-inflammatory microRNA, in vitro reports show anti-inflammatory effects in lipid-loaded cells. In this study we examined the role of miR155 in atherosclerosis in vivo using bone marrow transplantation from miR155 deficient or wildtype mice to hyperlipidemic mice. Hematopoietic deficiency of miR155 enhanced atherosclerotic plaque development and decreased plaque stability, as evidenced by increased myeloid inflammatory cell recruitment to the plaque. The increased inflammatory state was mirrored by a decrease in circulating CD4(+)CD25(+)FoxP3(+) regulatory T cells, and an increase in granulocytes (CD11b(+)Ly6G(+)) in blood of miR155(-/-) transplanted mice. Moreover, we show for the first time a crucial role of miR155 in monocyte subset differentiation, since hematopoietic deficiency of miR155 increases the 'inflammatory' monocyte subset (CD11b(+)Ly6G(-)Ly6C(hi)) and reduces 'resident' monocytes (CD11b(+)Ly6G(-)Ly6C(low)) in the circulation. Furthermore, cytokine production by resident peritoneal macrophages of miR155(-/-) transplanted hyperlipidemic mice was skewed towards a more pro-inflammatory state since anti-inflammatory IL-10 production was reduced. In conclusion, in this hyperlipidemic mouse model miR155 acts as an anti-inflammatory, atheroprotective microRNA. Additionally, besides a known role in lymphoid cell development, we show a crucial role of miR155 in myeloid lineage differentiation.