ArticlePLoS pathogens2018
PGL I expression in live bacteria allows activation of a CD206/PPARγ cross-talk that may contribute to successful Mycobacterium leprae colonization of peripheral nerves.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 33 citations in OpenAlex.
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- What happens when Schwann cells are exposed toIBRO neuroscience reports · 2023Review
- Single-cell sequencing analysis reveals development and differentiation trajectory of Schwann cells manipulated by M. leprae.PLoS neglected tropical diseases · 2023Article
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- Modulation of the Response toFrontiers in microbiology · 2022Review
- Functions of Stress-Induced Lipid Droplets in the Nervous System.Frontiers in cell and developmental biology · 2022Review
- Gene Expression Profile ofFrontiers in medicine · 2022Article
- Kynurenines in the Pathogenesis of Peripheral Neuropathy During Leprosy and COVID-19.Frontiers in cellular and infection microbiology · 2022Review
- Essential Roles of PPARs in Lipid Metabolism during Mycobacterial Infection.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Mycobacterium leprae, an obligate intracellular bacillus, infects Schwann cells (SCs), leading to peripheral nerve damage, the most severe leprosy symptom. In the present study, we revisited the involvement of phenolic glycolipid I (PGL I), an abundant, private, surface M. leprae molecule, in M. leprae-SC interaction by using a recombinant strain of M. bovis BCG engineered to express this glycolipid. We demonstrate that PGL I is essential for bacterial adhesion and SC internalization. We also show that live mycobacterium-producing PGL I induces the expression of the endocytic mannose receptor (MR/CD206) in infected cells in a peroxisome proliferator-activated receptor gamma (PPARγ)-dependent manner. Of note, blocking mannose recognition decreased bacterial entry and survival, pointing to a role for this alternative recognition pathway in bacterial pathogenesis in the nerve. Moreover, an active crosstalk between CD206 and the nuclear receptor PPARγ was detected that led to the induction of lipid droplets (LDs) formation and prostaglandin E2 (PGE2), previously described as fundamental players in bacterial pathogenesis. Finally, this pathway was shown to induce IL-8 secretion. Altogether, our study provides evidence that the entry of live M. leprae through PGL I recognition modulates the SC phenotype, favoring intracellular bacterial persistence with the concomitant secretion of inflammatory mediators that may ultimately be involved in neuroinflammation.
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