ABSTRACT
The metabolic pathway of cholesterol degradation by bacteria has not been completely established. Several possible intermediates have not been identified and many pathway delineations have not involved the use of the cholesterol molecule per se and just one bacterial species. The bacterial degradation of cholesterol by Pseudomonas sp. NCIB has been studied. Major biotransformation products included cholest-5-en-3-one, cholest-4-en-3-one, 26-hydroxycholest-4-en-3-one, androsta-1, 4-dien-3-17-dione, cholest-4-en-3-one-26-oic acid, chol-4-en-3-one-24-oic acid, pregn-4-en-3-one-20-carboxylic acid, and pregna-1, 4-dien-3-one-20-carboxylic acid. Studies with selected intermediates have enabled the elucidation of a comprehensive pathway of cholesterol degradation by bacteria.
November 1983 The Journal of Lipid Research, 24, 1500-1511.
http://www.jlr.org/content/24/11/1500.short
Mycobacterial persistence requires the utilization of host cholesterol
1. Amit K. Pandey and 2. Christopher M. Sassetti *
+Author Affiliations
1. Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655
1. Edited by Barry R. Bloom, Harvard School of Public Health, Boston, MA, and approved January 22, 2008 (received for review November 26, 2007)
Abstract
A hallmark of tuberculosis is the ability of the causative agent, Mycobacterium tuberculosis, to persist for decades despite a vigorous host immune response. Previously, we identified a mycobacterial gene cluster, mce4, that was specifically required for bacterial survival during this prolonged infection. We now show thatmce4 encodes a cholesterol import system that enables M. tuberculosis to derive both carbon and energy from this ubiquitous component of host membranes.