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首页> 外文期刊>Cytokine >Candida albicans SC5314 inhibits NLRP3/NLRP6 inflammasome expression and dampens human intestinal barrier activity in Caco-2 cell monolayer model
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Candida albicans SC5314 inhibits NLRP3/NLRP6 inflammasome expression and dampens human intestinal barrier activity in Caco-2 cell monolayer model

机译：Cancida albicans SC5314抑制Caco-2细胞单层模型中的NLRP3 / NLRP6炎症和抑制人类肠道阻隔活性

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摘要

Candida albicans is an opportunistic fungal pathogen that colonizes human gastro-intestinal mucosal tissues. Its effect on the immune response in intestinal epithelial cells and on the intestinal mucosal barrier are not yet fully understood. In this study, we investigated Caco-2 cells, a monolayer model of intestinal epithelial cells, with or without treatment with C. albicans SC5314 (CA) or heat-inactivated CA (CA-inact). RNA sequencing was conducted, and the mRNA and protein levels of NOD-like receptor pyrin domain-containing protein 3 (NLRP3) or NLRP6/ASC/caspase-1 inflammasome signaling pathway components, inflammatory cytokines (interleukin-18 [IL-18] and IL-1 beta), anti-microbial peptides (AMPs; beta-defensin-2 [BD-2], BD-3, and LL-37), and tight junction proteins (occludin and zona occludens-1 [ZO-1]) were examined by real-time PCR, western blotting, and/or immunofluorescence microscopy. Lactase dehydrogenase (LDH) activity in the Caco-2 cell supernatant were measured by enzyme kinetics analysis. Our results showed that the NOD-like receptor signaling pathway participates in the CA- and CA-inact-infected Caco-2 cells, as shown by microarray analysis of total mRNA expression. The expression of NLRP3, NLRP6, ASC, BD-2, BD-3, occludin, and ZO-1 were significantly decreased in Caco-2 cells infected with CA and CA-inact compared to that in the untreated control. IL-1 beta expression was decreased in the Caco-2 cells in both the CA- and CA-inact-infected groups compared to that in the control. Caspase-1 and IL-18 levels were not markedly affected by CA or CA-inact in Caco-2 cells. Our findings indicate that CA can inhibit the NLRP3 and NLRP6 pathways and dampen human intestinal mucosal barrier activity by decreasing the production of AMPs and tight junction proteins, independent of CA activity.
机译：念珠菌白醛本身是一种机会主义的真菌病原体，殖民殖民肠道粘膜组织。它对肠上皮细胞和肠粘膜屏障对免疫应答的影响尚未完全理解。在本研究中，我们研究了CaCo-2细胞，肠上皮细胞的单层模型，有或没有用C. albicans SC5314（Ca）或热灭活的Ca（Ca-minact）。进行RNA测序，以及含有点状受体吡林域蛋白3（NLRP3）或NLRP6 / ASC / CASPASE-1炎性细胞因子（白细胞介素-18 [IL-18]和IL-1β），抗微生物肽（AMPS; Beta-Defensin-2 [BD-2]，BD-3和LL-37）和紧密结蛋白（Occludin和Zona Occludens-1 [ZO-1]通过实时PCR，Western印迹和/或免疫荧光显微镜检查）检查。通过酶动力学分析测量CaCO-2细胞上清液中的乳糖酶脱氢酶（LDH）活性。我们的结果表明，NOD样受体信号传导途径参与CA-和CA-无与伦比的CACO-2细胞，如总mRNA表达的微阵列分析所示。与未处理的对照中的相比，在CaCo-2细胞中，NLRP3，NLRP6，ASC，BD-2，BD-3，OCCLUDIN和ZO-1的表达显着降低。与对照中的相比，在CA-和CA-无关的组中，在Ca-和Ca-和Ca-an-Ca-Mactoact的基团中，IL-1β表达在CaCo-2细胞中降低。 Caspase-1和IL-18水平未受CaCo-2细胞中的Ca或Ca-Detacc的显着影响。我们的研究结果表明，Ca通过减少与Ca活性无关的抑制安培和紧密结蛋白的产生，可以抑制NLRP3和NLRP6途径和抑制人肠粘膜屏障活性。

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  • 来源
    《Cytokine》 |2020年第2020期|共7页
  • 作者

    Mao Xiaqiong; Qiu Xinyun; Jiao Chunhua; Lu Meijiao; Zhao Xiaojing; Li Xueting; Li Jiajia; Ma Jingjing; Zhang Hongjie;

  • 作者单位

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

    Nanjing Med Univ Affiliated Hosp 1 Dept Gastroenterol Nanjing Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Candida; Intestinal barrier; Inflammasome; Antimicrobial peptides; Tight junction proteins;

    机译：念珠菌;肠道屏障;炎症;抗微生物肽;紧密结蛋白;

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