Abstract
We isolated a rough variant of Mycobacterium abscessus CIP 104536T during experimental infection of mice. We show that this variant has lost the ability to produce glycopeptidolipids, is hyperlethal for C57BL/6 mice infected intravenously, and induces a strong tumor necrosis factor-alpha response by murine monocyte-derived macrophages.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Disease Models, Animal
-
Glycolipids / biosynthesis
-
Glycopeptides / biosynthesis
-
Macrophages / immunology
-
Mice
-
Mice, Inbred C57BL
-
Mutation
-
Mycobacterium Infections, Nontuberculous / immunology
-
Mycobacterium Infections, Nontuberculous / microbiology*
-
Mycobacterium chelonae / immunology
-
Mycobacterium chelonae / pathogenicity*
-
Mycobacterium chelonae / physiology
-
Survival Analysis
-
Tumor Necrosis Factor-alpha / biosynthesis
-
Virulence
Substances
-
Glycolipids
-
Glycopeptides
-
Tumor Necrosis Factor-alpha