KLF4 is involved in secondary Echinococcus granulosus infection

What is it about?

The objective of this study was to investigate macrophage polarization during the early stages of secondary Echinococcus granulosus sensu lato (E. granulosus s.l.) infection. We observed an early initial increase in inflammatory genes (peaking at 5-10 days) and a later rise in M (IL-4)-like genes (still rising by day 15). In addition, we showed that the induction of M (IL-4) –like genes were paralleled by an increase in expression of the transcription factor KLF4.Most of the changes observed in vivo were reproduced in vitro upon the culture of normal peritoneal macrophages with live E. granulosus s.l. protoscoleces (PSC), and that knockdown of KLF4 in this system attenuates M (IL-4) differentiation. Our results suggest that KLF4 pathway contributes to the differentiation of macrophages towards M (IL-4)-like phenotype during early stages of secondary E.granulosus s.l. infection.

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Why is it important?

In this study, we showed that PSC-induced macrophage polarization towards an M (IL-4)-like phenotype and discovered that increased expression of KLF4 on macrophages is associated with alternative macrophage activation during the secondary model of E. granulosus s.l. infection.This model has disadvantages: it does not reproduce the primary infection (caused by the ingestion of oncospheres) and uses a non-natural host. Therefore, different mechanisms may be involved in the induction/resolution of inflammation during the establishment of oncospheres in viscera of a natural host . No matter what, our data may report at least a novel observation between E. granulosus s.l. and macrophage activation, because, macrophage activation has been very well demonstrated for other helminth infections.

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