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Background    Toxoplasma gondii  can invade and replicate in all nucleated cells in a wide range of host species, and infection induces IL-1β production. IL-1β plays central roles in the stimulation of the innate immune system and inflammation. However, little is known of the innate immune responses in human fetal small intestinal epithelial cells (FHs 74 Int cells) after  T. gondii  infection.    Methods  FHs 74 Int cells were infected with the  T. gondii  GFP-RH strain. Then, IL-1β production and its mechanisms of action were evaluated using ELISA, MTT cell viability assays, Western blotting, immunofluorescence, quantitative real-time polymerase chain reaction (qRT-PCR), and gene-specific small interfering RNA (siRNA) transfection.    Results  Infection of FHs 74 Int cells by  T. gondii  triggered significant time- and dose-dependent IL-1β production. Although  T. gondii  activated NLRP1, NLRP3, NLRC4 and AIM2 inflammasomes in FHs 74 Int cells, NLRP3 levels were consistently and significantly time-dependently increased, while the other inflammasomes were not. Transfection with siRNA targeting NLRP3, cleaved caspase-1 (Casp-1) or ASC significantly reduced  T. gondii -induced IL-1β production, whereas  T. gondii  proliferation was markedly increased.  Toxoplasma gondii  infection activated P2X7 receptor (P2X7R) levels in FHs 74 Int cells in a time-dependent manner; however, transfection with siRNA targeting P2X7R significantly reduced  T. gondii -induced IL-1β secretion and substantially increased  T. gondii  proliferation, which is mediated by decreased protein expression levels of NLRP3, cleaved Casp-1 and ASC. Collectively, NLRP3-dependent IL-1β secretion is mediated by P2X7R in small intestinal epithelial cells in response to  T. gondii  infection, thereby controlling parasite proliferation.    Conclusions  This study revealed that the P2X7R/NLRP3 pathway plays important roles in IL-1β secretion and inhibition of  T. gondii  proliferation in small intestinal epithelial cells. These results not only contribute to our understanding of the mucosal immune mechanisms of  T. gondii  infection but also offer new insight into the identification of innate resistance in the gut epithelium.    Electronic supplementary material  The online version of this article (10.1186/s13071-017-2573-y) contains supplementary material, which is available to authorized users.

parasites and vectors

P2X7 receptor mediates NLRP3-dependent IL-1β secretion and parasite proliferation in Toxoplasma gondii-infected human small intestinal epithelial cells