{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T19:52:55Z","timestamp":1790452375490,"version":"4.1.0"},"reference-count":77,"publisher":"Public Library of Science (PLoS)","issue":"10","license":[{"start":{"date-parts":[[2024,10,22]],"date-time":"2024-10-22T00:00:00Z","timestamp":1729555200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100015310","name":"Natural Science Foundation of Xinjiang","doi-asserted-by":"publisher","award":["2023D01A120"],"award-info":[{"award-number":["2023D01A120"]}],"id":[{"id":"10.13039\/501100015310","id-type":"DOI","asserted-by":"publisher"}]},{"name":"the Key R&D Programme Projects of Xinjiang Uygur Autonomous Region, China","award":["2022B03013-4"],"award-info":[{"award-number":["2022B03013-4"]}]},{"name":"State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia - The Third People's Hospital of Xinjiang Uygur Autonomous Region Joint Fund projects","award":["SKL-HIDCA-2023-MK12"],"award-info":[{"award-number":["SKL-HIDCA-2023-MK12"]}]}],"content-domain":{"domain":["www.plosntds.org"],"crossmark-restriction":false},"short-container-title":["PLoS Negl Trop Dis"],"abstract":"<jats:sec id=\"sec001\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Cystic\n                      <jats:italic>Echinococcosis<\/jats:italic>\n                      (CE) is a zoonotic disease causing fibrosis and necrosis of diseased livers caused by infection with\n                      <jats:italic>Echinococcus granulosus<\/jats:italic>\n                      (\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      ). There is evidence that\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      is susceptible to immune escape and tolerance when host expression of immunoinflammation and fibrosis is suppressed, accelerating the progression of CE. Ghrelin has the effect of suppressing immunoinflammation and fibrosis, and whether it is involved in regulating the progression of\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      -infected liver lesions is not clear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec002\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Serum and hepatic Ghrelin levels were observed in\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      -infected mice (4, 12 and 36 weeks) and compared with healthy control groups. Co-localization analysis is performed between protein expression of Ghrelin in and around the hepatic lesions of\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      -infected 12-week mice and protein expression of different hepatic histiocytes by mIHC. HepG2 cells and protoscoleces (PSCs) protein were co-cultured in vitro, as well as PSCs were alone in vitro, followed by exogenously administered of Ghrelin and its receptor blocker, [D-Lys3]-GHRP-6, to assess their regulatory effects on immunoinflammation, fibrosis and survival rate of PSCs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec003\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Serum Ghrelin levels were increased in\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      -infected 4- and 12-week mice, and reduced in 36-week mice.\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      -infected mice consistently recruited Ghrelin in and around the hepatic lesions, which was extremely strongly co-localized with the protein expression of hepatic stellate cells (HSCs), T cells and the TGF-\u03b21\/Smad3 pathway. The secretion of Ghrelin was increased with increasing concentrations of PSCs protein in HepG2 cells culture medium. Moreover, Ghrelin could significantly inhibit the secretion of IL-2, INF-\u03b3 and TNF-\u03b1, as well as the expression of Myd88\/NF-\u03baB and TGF-\u03b21\/Smad3 pathway protein, and promoted the secretion of IL-4 and IL-10. Blocking Ghrelin receptor could significantly inhibit PSCs growth in\n                      <jats:italic>in vitro<\/jats:italic>\n                      experiment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec004\">\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Ghrelin is highly expressed in the early stages of hepatic\n                      <jats:italic>E<\/jats:italic>\n                      .\n                      <jats:italic>g<\/jats:italic>\n                      infection and may be involved in regulating the progression of liver lesions by suppression immunoinflammation and fibrosis.\n                    <\/jats:p>\n                  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