Article
Indoleamine 2,3-dioxygenase and iron are required for Mycobacterium leprae survival
Registro en:
BARBOSA, Mayara Garcia de Mattos; et al. Indoleamine 2,3-dioxygenase and iron are required for Mycobacterium leprae survival. Microbes and Infection, v.19, p.505-514, 2017.
1286-4579
10.1016/j.micinf.2017.06.006
1769-714X
Autor
Barbosa, Mayara Garcia de Mattos
Prata, Rhana Berto da Silva
Andrade, Priscila Ribeiro
Ferreira, Helen
Silva, Bruno Jorge de Andrade
Oliveira, Jéssica Araújo
Assis, Tayná Quintella da Paixão de
Pinto, Thiago Gomes de Toledo
Bezerra, Ohanna Cavalcanti de Lima
Nery, José Augusto da Costa
Rosa, Patricia Sammarco
Bozza, Marcelo Torres
Lara, Flavio Alves
Moraes, Milton Ozório
Schmitz, Veronica
Sarno, Euzenir Nunes
Pinheiro, Roberta Olmo
Resumen
Our previous study has demonstrated that IL-10 may modulate both indoleamine 2,3-dioxygenase (IDO) and CD163 expression in lepromatous leprosy (LL) cells, favoring Mycobacterium leprae persistence through induction of regulatory pathways and iron storage. Here, we observed that in LL lesion cells there is an increase in the expression of proteins involved in iron metabolism such as hemoglobin (Hb), haptoglobin, heme oxygenase 1 and transferrin receptor 1 (TfR1) when compared to tuberculoid leprosy (BT) cells. We also found increased iron deposits and diminished expression of the iron exporter ferroportin 1 in LL lesion cells. Hemin, but not FeSO4 stimulation, was able to enhance M. leprae viability by a mechanism that involves IDO. Analysis of cell phenotype in lesions demonstrated a predominance of M2 markers in LL when compared with BT lesion cells. A positive correlation between CD163 and PPARG with the bacillary index (BI) was observed. In contrast, TNF, STAT1 and CSF2 presented a negative correlation with the BI. In summary, this study demonstrates that iron may regulate IDO expression by a mechanism that involves IL-10, which may contribute for the predominance of M2-like phenotype in LL lesions that favors the phagocytosis and maintenance of M. leprae in host cells. 2030-01-01