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.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Díaz Acosta CC,Dias AA,Rosa TLSA,Batista-Silva LR,Rosa PS,Toledo-Pinto TG,Costa FDMR,Lara FA,Rodrigues LS,Mattos KA,Sarno EN,Bozza PT,Guilhot C,de Berrêdo-Pinho M,Pessolani MCVdoi
10.1371/journal.ppat.1007151subject
Has Abstractpub_date
2018-07-06 00:00:00pages
e1007151issue
7eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-18-00369journal_volume
14pub_type
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