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Díaz Acosta, Chyntia Carolina; Dias, André Alves; Rosa, Thabatta Leal Silveira Andrezo; Batista-Silva, Leonardo Ribeiro; Rosa, Patricia Sammarco; Toledo-Pinto, Thiago Gomes; Costa, Fabrício da Mota Ramalho; Lara, Flávio Alves; Rodrigues, Luciana Silva; Mattos, Katherine Antunes; Sarno, Euzenir Nunes; Bozza, Patrícia Torres; Guilhot, Christophe; de Berrêdo-Pinho, Márcia; Pessolani, Maria Cristina Vidal
PLoS pathogens, 07/2018, Volume: 14, Issue: 7Journal Article
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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