{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T06:49:43Z","timestamp":1790232583929,"version":"4.1.0"},"reference-count":65,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2017,11,16]],"date-time":"2017-11-16T00:00:00Z","timestamp":1510790400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Innate Immun"],"published-print":{"date-parts":[[2018,1]]},"abstract":"<jats:p>Inflammasome-mediated production of mature IL-1\u03b2 and IL-18 cytokines represents an important innate immune response against infecting pathogens. Helicobacter pylori, one of the most successful and persistent human pathogens, induces severe inflammation leading to gastritis and more serious gastric diseases. H. pylori modulates different immune responses for its survival and inflammasome signaling is manipulated by the cag pathogenicity island ( cagPAI), urease and VacA cytotoxin. Here we report that H. pylori regulates NLRP3 expression, an inflammasome forming regulator, in infected THP-1 monocytes. This response was independent of the major H. pylori pathogenicity-associated factors CagA, VacA, Cgt, FlaA and cagPAI. Two NLRP3 expression controlling factors, the NLRP3 mRNA targeting microRNA hsa-miR-223-3p and cytokine IL-10, were found to work in tandem for its regulation. H. pylori infection also induced copious amount of pro-IL-1\u03b2 in THP-1 monocytes\/macrophages but secreted a very low amount of mature IL-1\u03b2. Moreover, secreted IL-10 correlated with the down-regulation of nigericin-induced NLRP3 inflammasome activation of LPS-primed THP-1 monocytes and human PBMCs from volunteers. However, H. pylori-treated PBMCs secreted significantly more mature IL-1\u03b2 throughout the infection period, which suggests a different mode of activation. Taken together, this study demonstrates targeting of inflammasome-forming NLRP3, an important innate immunity component, and crucial manipulation of pro- and anti-inflammatory cytokines in H. pylori infection.<\/jats:p>","DOI":"10.1177\/1753425917738043","type":"journal-article","created":{"date-parts":[[2017,11,17]],"date-time":"2017-11-17T00:45:33Z","timestamp":1510879533000},"page":"11-23","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":50,"title":["<i>Helicobacter pylori<\/i>\n                    controls NLRP3 expression by regulating hsa-miR-223-3p and IL-10 in cultured and primary human immune cells"],"prefix":"10.1177","volume":"24","author":[{"given":"Suneesh Kumar","family":"Pachathundikandi","sequence":"first","affiliation":[{"name":"Division of Microbiology, Department of Biology, Friedrich Alexander University, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steffen","family":"Backert","sequence":"additional","affiliation":[{"name":"Division of Microbiology, Department of Biology, Friedrich Alexander University, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2017,11,16]]},"reference":[{"key":"bibr1-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1159\/000235763"},{"key":"bibr2-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro3016"},{"key":"bibr3-1753425917738043","doi-asserted-by":"publisher","DOI":"10.2217\/fmb.15.32"},{"key":"bibr4-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2007.11.009"},{"key":"bibr5-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1172\/JCI38605"},{"key":"bibr6-1753425917738043","doi-asserted-by":"publisher","DOI":"10.4161\/gmic.27001"},{"key":"bibr7-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.00054-05"},{"key":"bibr8-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1172\/JCI61029"},{"key":"bibr9-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1097\/MIB.0000000000000318"},{"key":"bibr10-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1172\/JCI79337"},{"key":"bibr11-1753425917738043","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2016.00071"},{"key":"bibr12-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1038\/35006081"},{"key":"bibr13-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1007\/s10555-006-9004-4"},{"key":"bibr14-1753425917738043","doi-asserted-by":"publisher","DOI":"10.1007\/s10120-014-0448-x"},{"key":"bibr15-1753425917738043","doi-asserted-by":"crossref","unstructured":"Backert, S.\n                      Inflammasome signaling and bacterial infections\n                      . 1st ed. 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Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome.\n                      J Exp Med\n                      2017; 214: 1737\u20131752.","DOI":"10.1084\/jem.20160462"},{"key":"bibr61-1753425917738043","doi-asserted-by":"crossref","unstructured":"Ma L, Chen Y, Zhang B, et al. 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