Cholesterol plays a larger role during Mycobacterium tuberculosis in vitro dormancy and reactivation than previously suspected.

摘要: It is known that cholesterol plays a key role for Mycobacterium tuberculosis (Mtb) adaptation and survival within the host, thus contributing to establishment of dormancy. has been extensively demonstrated fatty acids are main energy source Mtb during infection dormancy, it proposed these molecules implicated in reactivation bacilli from dormant state. We used in vitro models analyze gene expression dormancy when unique carbon media. Our results suggest might function as signal trigger some genes required stress protection earlier than one induced by alone, indicating very favorable its development. This process so conducive cholesterol-adapted can reactivate their growth after NRP2 state even 10 min post ventilation. Thus, we hypothesize not only involved but also critical almost immediate an long-lasting hypoxia.