Dissecting the membrane cholesterol requirement for mycobacterial entry into host cells

摘要: Mycobacteria are intracellular pathogens that can invade and survive within host macrophages, a major cause of mortality morbidity worldwide. The molecular mechanism involved in the internalization mycobacteria is poorly understood. In this work, we have explored role membrane cholesterol entry avirulent surrogate mycobacterial strain Mycobacterium smegmatis into THP-1 macrophages. Our results show depletion using methyl-β-cyclodextrin significant reduction M. cells. More importantly, inhibition ability to enter macrophages could be reversed upon replenishment cholesterol. To best our knowledge, these constitute first report showing reverse addition, demonstrate complexation amphotericin B (without physical depletion) sufficient inhibit entry. Importantly, observed enrichment Taken together, demonstrate, for time, an optimum plasma necessary mycobacteria. These assume relevance context developing novel therapeutic strategies targeting cholesterol-mediated cell