Expression profiles of NOD-like receptors and regulation of NLRP3 inflammasome activation in Toxoplasma gondii-infected human small intestinal epithelial cells.
Expression profiles of NOD-like receptors and regulation of NLRP3 inflammasome activation in Toxoplasma gondii-infected human small intestinal epithelial cells.
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弓形虫感染的人小肠上皮细胞中 NOD 样受体的表达谱及 NLRP3 炎症小体激活的调节
DOI：
10.1186/s13071-021-04666-w
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发表时间：
2021-03-12
影响因子：
3.2
通讯作者：
Lee YH
中科院分区：
文献类型：
--
作者：
Chu JQ;Gao FF;Wu W;Li C;Pan Z;Sun J;Wang H;Huang C;Lee SH;Quan JH;Lee YH
刚地弓形虫是一种主要通过口腔途径感染的寄生虫。核苷酸结合寡聚化结构域（NOD）样受体（NLR）在寄生虫感染期间产生的免疫应答中起关键作用，并且还驱动针对入侵寄生虫的炎症应答。然而，对T细胞中NLR和炎性小体激活的调控知之甚少。刚地虫感染的人小肠上皮（FH 74 Int）细胞。FH 74 Int细胞感染T.随后评价了弓形虫的形态学变化、细胞毒性、NLR的表达谱、炎性体组分、半胱天冬酶切割的白细胞介素（IL）以及NLRP 3和NLRP 6炎性体活化的机制。采用免疫细胞化学、乳酸脱氢酶测定、逆转录聚合酶链反应（RT-PCR）、实时定量RT-PCR和蛋白质印迹技术进行分析。在正常和T.在弓形虫感染的条件下，除了NLRC 3、NLRP 5和NLRP 9之外，NLR的成员、炎性体组分和半胱天冬酶切割的IL在FH Int 74细胞中表达。在NLR中，NOD 2、NLRP 3、NLRP 6和NAIP 1的mRNA表达在T.而NLRP 2、NLRP 7和CIITA mRNA的表达以时间依赖性方式显著降低。此外，T.在FH 74 Int细胞中，弓形虫感染诱导NLRP 3、NLRP 6和NLRC 4炎性体活化以及IL-1β、IL-18和IL-33的产生。T. gondii诱导的NLRP 3炎性小体激活与p38 MAPK的磷酸化密切相关;然而，JNK 1/2的作用较弱。在FH 74 Int细胞中，NLRP 6炎性体活化与MAPK通路无关。本研究着重阐明了NLR的表达谱，并阐明了NLRP 3炎性小体在T.刚地虫感染的FH 74 Int细胞。这些发现可能有助于理解T.在FH 74 Int细胞中的弓形虫感染。
Toxoplasma gondii is a parasite that primarily infects through the oral route. Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) play crucial roles in the immune responses generated during parasitic infection and also drive the inflammatory response against invading parasites. However, little is known about the regulation of NLRs and inflammasome activation in T. gondii-infected human small intestinal epithelial (FHs 74 Int) cells. FHs 74 Int cells infected with T. gondii were subsequently evaluated for morphological changes, cytotoxicity, expression profiles of NLRs, inflammasome components, caspase-cleaved interleukins (ILs), and the mechanisms of NLRP3 and NLRP6 inflammasome activation. Immunocytochemistry, lactate dehydrogenase assay, reverse transcription polymerase chain reaction (RT-PCR), real-time quantitative RT-PCR, and western blotting techniques were utilized for analysis. Under normal and T. gondii-infected conditions, members of the NLRs, inflammasome components and caspase-cleaved ILs were expressed in the FHs Int 74 cells, except for NLRC3, NLRP5, and NLRP9. Among the NLRs, mRNA expression of NOD2, NLRP3, NLRP6, and NAIP1 was significantly increased in T. gondii-infected cells, whereas that of NLRP2, NLRP7, and CIITA mRNAs decreased significantly in a time-dependent manner. In addition, T. gondii infection induced NLRP3, NLRP6 and NLRC4 inflammasome activation and production of IL-1β, IL-18, and IL-33 in FHs 74 Int cells. T. gondii-induced NLRP3 inflammasome activation was strongly associated with the phosphorylation of p38 MAPK; however, JNK1/2 had a weak effect. NLRP6 inflammasome activation was not related to the MAPK pathway in FHs 74 Int cells. This study highlighted the expression profiles of NLRs and unraveled the underlying mechanisms of NLRP3 inflammasome activation in T. gondii-infected FHs 74 Int cells. These findings may contribute to understanding of the mucosal and innate immune responses induced by the NLRs and inflammasomes during T. gondii infection in FHs 74 Int cells.
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影响因子：
4.7
作者：
Nagyoszi, Peter;Nyul-Toth, Adam;Krizbai, Istvan A.
通讯作者：
Krizbai, Istvan A.
影响因子：
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影响因子：
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