MyD88-dependent pathway is essential for the innate immunity to Enterocytozoon bieneusi.

MyD88-dependent pathway is essential for the innate immunity to Enterocytozoon bieneusi.
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DOI:
10.1111/j.1365-3024.2010.01269.x
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发表时间:
2011-04
影响因子:
2.2
通讯作者:
Feng H
Feng H
中科院分区:
医学4区
文献类型:
--
作者:
Zhang Q;Feng X;Nie W;Golenbock DT;Mayanja-Kizza H;Tzipori S;Feng H

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Enterocytozoon bieneusi is clinically the most significant microsporidian parasite associated with persistent diarrhea, wasting and cholangitis in 30-50% of individuals with HIV/AIDS, as well as in malnutritional children and in recipients of immunosuppressive therapy. However, the host immune responses to E. bieneusi have not been investigated until recently due to lack of sources of spores, cell culture system, and animal models. In this study, we purified spores from heavily infected human or monkey feces by serial salt-Percoll-sucrose-iodixanol centrifugation and the purity of spores was confirmed by FACS and scanning electron microscopy. Exposure of dendritic cells to E. bieneusi spores induced up-regulation of the surface markers and production of pro-inflammatory cytokines. The cytokine production was independent of Toll-like receptor 4, but MyD88-dependent, since dendritic cells from MyD88 knockout mice failed to secrete these pro-inflammatory cytokines, whereas dendritic cells from C3H/HeJ (a Toll-like receptor 4 mutant) were activated by E. bieneusi and secreted these cytokines. Furthermore, MyD88 deficient mice were susceptible to E. bieneusi infection, in contrast to wild type mice which resisted the infection. Collectively the data demonstrate innate recognition of E. bieneusi by dendritic cells and the importance of MyD88-dependent signaling in resisting infection in a murine challenge model.
Toll样受体9介导疟疾色素血液唑素的先天免疫激活。
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