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Review
. 2021 Feb 25;17(2):e1009253.
doi: 10.1371/journal.ppat.1009253. eCollection 2021 Feb.

New insights into the interactions between Blastocystis, the gut microbiota, and host immunity

Affiliations
Review

New insights into the interactions between Blastocystis, the gut microbiota, and host immunity

Lei Deng et al. PLoS Pathog. .

Abstract

The human gut microbiota is a diverse and complex ecosystem that is involved in beneficial physiological functions as well as disease pathogenesis. Blastocystis is a common protistan parasite and is increasingly recognized as an important component of the gut microbiota. The correlations between Blastocystis and other communities of intestinal microbiota have been investigated, and, to a lesser extent, the role of this parasite in maintaining the host immunological homeostasis. Despite recent studies suggesting that Blastocystis decreases the abundance of beneficial bacteria, most reports indicate that Blastocystis is a common component of the healthy gut microbiome. This review covers recent finding on the potential interactions between Blastocystis and the gut microbiota communities and its roles in regulating host immune responses.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Blastocystis-mediated regulation of immune responses and homeostasis as characterized by studies using in vitro systems and experimental rodent models.
This illustration simplifies the many interactions and pathways involved in Blastocystis colonization or infection in host cells. Cysteine proteases produced by Blastocystis are able to degrade IgA and AMP (LL-37). Blastocystis can also influence the gene expression of pro-inflammatory cytokines by regulating the NF-κB and MAPK pathways. Blastocystis evades host NO antiparasitic response by inhibiting iNOS to convert arginine to NO. Blastocystis can induce Th1 and Th17 cells responses and their signature cytokines release. AMP, antimicrobial peptide; GM-CSF, granulocyte-macrophage colony-stimulating factor; IFNγ, interferon gamma; IgA, immunoglobulin A; IL, interleukin; iNOS, inducible nitric oxide synthase; L-Arg, L-Arginine; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-κB; NO, nitric oxide; Th, T helper; TNFα, tumor necrosis factor alpha; ZO1, zonula occludens-1.

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