About this Research Topic
The mortality and spread of tuberculosis (TB) has been further aggravated by the alarming rise in multidrug-, extensively drug- and totally drug-resistant cases. In 2015, 10.4 million new cases of active TB have been reported resulting in 1.8 million deaths. Nevertheless, the WHO has vowed to reduce TB morbidity by 90% and TB mortality by 95% by 2035. This ambitious goal can only be successfully accomplished if more rapid diagnostics, effective treatment and prevention strategies are made available for pulmonary TB.
In particular, there is a widely acknowledged need for novel biomarkers at all stages of TB: diagnosis, treatment and prevention. Therefore, more efforts to discover new potential targets are needed in order to reduce/control the expansion of the disease. In this context, exploring bacterial enzymes involved in lipid metabolism could highlight targets playing major roles in the physiopathology of the bacterium. Its unique cell wall architecture is indeed composed of complex lipids (including mycolic acids, phosphatidylinositol mannosides, phthiocerol dimycocerosates, lipoglycans…), and a lipid accumulation process is occurring during its lifetime within the host, showing the importance of the lipid metabolism in M. tuberculosis virulence and persistence processes.
The central feature of M. tuberculosis pathogenesis is its ability to escape macrophage killing, and to induce the appearance of granulomatous lesions populated with foamy macrophages (FM). These specific FM contain a large amount of cytoplasmic lipid bodies (LB), mainly composed of triacylglycerols, allowing bacilli to accumulate lipids as intracytoplasmic lipid inclusions (ILI). Such ILIs are thought to be essential for persistence, leading to latent TB, as they can provide the bacillus with energy via the β-oxidation pathway, during the chronic phase of infection and the reactivation step. During the later step, these ILIs may be degraded and supply precursors for the synthesis of bacterial cell membrane lipids, which play a key role in the replication and pathogenicity of M. tuberculosis.
The main objectives of this Research Topic is to highlight the most recent advances in the role and relationship between lipids and M. tuberculosis virulence and persistence. The Research Topic will include research articles dealing with the identification and characterization of proteins/genes involved in synthesis or degradation of lipids from bacterial or host cells, host-pathogen interaction between lipid-loaded cells/bacteria, new or revisited model organisms to investigate M. tuberculosis virulence and persistence, regulation of lipid metabolism, as well as new insights in the immunology of the lipid-rich cells/bacteria and histologic investigation of the occurrence of FM in granulomatous lesions.
This Research Topic will also be opened to other pathogenic mycobacteria, as well as other relevant research areas as long as they are related with lipids and their role in the host-pathogen relationship.
In particular, there is a widely acknowledged need for novel biomarkers at all stages of TB: diagnosis, treatment and prevention. Therefore, more efforts to discover new potential targets are needed in order to reduce/control the expansion of the disease. In this context, exploring bacterial enzymes involved in lipid metabolism could highlight targets playing major roles in the physiopathology of the bacterium. Its unique cell wall architecture is indeed composed of complex lipids (including mycolic acids, phosphatidylinositol mannosides, phthiocerol dimycocerosates, lipoglycans…), and a lipid accumulation process is occurring during its lifetime within the host, showing the importance of the lipid metabolism in M. tuberculosis virulence and persistence processes.
The central feature of M. tuberculosis pathogenesis is its ability to escape macrophage killing, and to induce the appearance of granulomatous lesions populated with foamy macrophages (FM). These specific FM contain a large amount of cytoplasmic lipid bodies (LB), mainly composed of triacylglycerols, allowing bacilli to accumulate lipids as intracytoplasmic lipid inclusions (ILI). Such ILIs are thought to be essential for persistence, leading to latent TB, as they can provide the bacillus with energy via the β-oxidation pathway, during the chronic phase of infection and the reactivation step. During the later step, these ILIs may be degraded and supply precursors for the synthesis of bacterial cell membrane lipids, which play a key role in the replication and pathogenicity of M. tuberculosis.
The main objectives of this Research Topic is to highlight the most recent advances in the role and relationship between lipids and M. tuberculosis virulence and persistence. The Research Topic will include research articles dealing with the identification and characterization of proteins/genes involved in synthesis or degradation of lipids from bacterial or host cells, host-pathogen interaction between lipid-loaded cells/bacteria, new or revisited model organisms to investigate M. tuberculosis virulence and persistence, regulation of lipid metabolism, as well as new insights in the immunology of the lipid-rich cells/bacteria and histologic investigation of the occurrence of FM in granulomatous lesions.
This Research Topic will also be opened to other pathogenic mycobacteria, as well as other relevant research areas as long as they are related with lipids and their role in the host-pathogen relationship.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
