Immunity and metabolism at the interface of mycobacteria and host
The mycobacteria causing Tuberculosis, Leprosy and Buruli ulcer constitute a major cause of mortality and morbidity worldwide. They have in common an ability to cause chronic, often latent, infections escaping host immune surveillance and protective immunity. The successful eradication of pathogenic mycobacteria requires patient adherence to long-term antibiotic therapies, with major side effects. Non-compliance to these treatments is frequent, leading to relapses, and the emergence of multi-drug resistant strains. Clearly, additional anti-mycobacterial strategies are needed to shorten antibiotic treatments and avoid the development of drug resistance.
A new approach that we have explored over the past few years is to target mycobacterial factors that suppress the development of protective immune responses. Currently our work is focused on mycolactone of Mycobacterium ulcerans, and phenolic glycolipids made by the Leprosy bacillus and hyper-virulent strains of the Tubercle bacillus. Research in our laboratory aims at understanding their mechanism of action, with a particular focus on how they deviate central metabolic pathways in immune cells. We are committed to translating our findings into novel approaches to prevent or treat mycobacterial diseases. Further, we hope that our work will lead to the identification of lead compounds targeting the metabolic control of immune cell functions.