MBEC Versus MBIC: the Lack of Differentiation between Biofilm Reducing and Inhibitory Effects as a Current Problem in Biofilm Methodology - 2019
Lara Thieme, Anita Hartung, Kristina Tramm, Mareike Klinger-Strobel, Klaus D. Jandt, Oliwia Makarewicz, Mathias W. Pletz
Abstract
Background
Biofilms are communities of aggregated, matrix-embedded microbial cells showing a high tolerance to an in principle adequate antibiotic therapy, often resulting in treatment failure. A major challenge in the management of biofilm-associated infections is the development of adequate, standardized biofilm susceptibility testing assays that are clinically meaningful, i.e. that their results correlate with treatment outcome. Different biofilm susceptibility endpoint parameters like the minimal biofilm eradication concentration (MBEC) or the minimal biofilm inhibitory concentration (MBIC) have been suggested as a guide for treatment of biofilm-associated infections, however with inconsistent perception and use among biofilm researchers, leading to confusion and contradictions among different anti-biofilm component studies and clinical trials.
Findings
Evaluation of anti-biofilm effects is mostly based on the untreated reference growth control biofilm measured at the same endpoint as the treated biofilm, neglecting the possible change of the untreated reference biofilm from the time point of pre-antimicrobial exposure to the measured endpoint. In this commentary, we point out the importance of individual quantification of mature, established biofilms before antimicrobial treatment for each biofilm model in order to draw conclusions on the measured biofilm effect size, i.e. biofilm reducing (MBEC) or biofilm inhibitory (MBIC) effects.
Conclusion
The assessment of pre-treatment biofilms contributes to a standardized use of biofilm susceptibility endpoint parameters, which is urgently needed to improve the clinical validity of future anti-biofilm assays.
Blockade of ITGA2 Induces Apoptosis and Inhibits Cell Migration in Gastric Cancer - 2018
Yu Chang Chuang, Chang-Jer Wu, Yuling Lin, Shey-Cherng Tzou, Ching-Te Chuang, Ting Yan Jian, Pin Rong Chen, Yuan Chang, Chi Hsin Lin, Tse-Hung Huang, Chao Ching Wang, Yi Lin Chan, Kuang‐Wen Liao
Endothelial Mesenchymal Transition: Comparative Analysis of Different Induction Methods Tập 18 - Trang 1-8 - 2016
Mariana T. Pinto, Dimas T. Covas, Simone Kashima, Claudia O. Rodrigues
Endothelial-Mesenchymal-Transition (EndMT) plays an essential role in cardiovascular development, and recently became an attractive therapeutic target based on evidence supporting its involvement in fibrosis and cancer. Important questions that remain to be answered are related to the molecular mechanisms that control EndMT in different organs and distinct pathological conditions. The lack of a detailed protocol for induction of EndMT and the assumption that TGF-β isoforms play similar roles on different types of endothelial cells, limit progress in the field. The aim of this study was to compare the induction of EndMT by TGF-β isoforms in endothelial cells of different sources, and define a detailed protocol for EndMT assessment in vitro. We compared the dose-dependent effect of TGF-β isoforms, under normoxia and hypoxia, on the induction of EndMT in human coronary and pulmonary artery endothelial cells. Our results suggest that endothelial cells undergo spontaneous EndMT with time in culture under the conditions tested. The extent of EndMT induction by TGF-β was dependent on the dose and endothelial cell type. Furthermore, the potential of TGF-β to induce EndMT was reduced under hypoxia relative to normoxia. Our work suggests that the response of endothelial cells to TGF-β is intrinsic to the dose, cell type and environment. Optimization of induction conditions may be essential, as pathways triggering EndMT may vary during development and pathological conditions. Therefore, caution is needed regarding indiscriminate use of TGF-β to induce EndMT for mechanistic studies.
