{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T05:10:30Z","timestamp":1788844230178,"version":"build-2803163510"},"reference-count":60,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T00:00:00Z","timestamp":1788825600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background and objective<\/jats:title>\n                    <jats:p>\n                      Alveolar echinococcosis (AE) is a fatal zoonotic parasitic disease that causes progressive hepatic injury through chronic inflammation, aberrant proliferative repair, and liver fibrosis. GHSR and TLR4 individually regulate hepatic inflammation and proliferation; however, their synergistic roles in\n                      <jats:italic>Echinococcus multilocularis<\/jats:italic>\n                      (\n                      <jats:italic>E. multilocularis<\/jats:italic>\n                      )-induced AE remain unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Wild-type (WT), GHSR-knockout (GHSR\n                      <jats:sup>-\/-<\/jats:sup>\n                      ), and TLR4-knockout (TLR4\n                      <jats:sup>-\/-<\/jats:sup>\n                      ) murine AE models were established, and comprehensive evaluations of hepatic pathology, cell proliferation, macrophage polarization, inflammatory factors, and hepatic proteomic profiles were performed at 12 weeks post-infection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Knockout of either GHSR or TLR4 alleviated AE-induced hepatic lesions, fibrosis, and liver dysfunction. Mechanistically, their deletion suppressed PI3K\/Akt-mediated proliferation and TLR4\/MyD88\/NF-\u03baB-mediated inflammation, reduced M1\/M2 macrophage infiltration, decreased pro-inflammatory cytokines (IL-6, TNF-\u03b1, and TGF-\u03b21), and elevated anti-inflammatory IL-10. A positive expression correlation between GHSR and TLR4 was confirmed in AE, Proteomics further verified their coordinated modulation of hepatic inflammation and aberrant repair.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Collectively, upregulated GHSR and TLR4 jointly promote Echinococcus multilocularis-associated hepatic damage via sustaining persistent inflammation and dysregulated proliferative tissue repair. This study demonstrates coordinated pro-pathological involvement of GHSR and TLR4 in AE progression and provides\n                      <jats:italic>in vivo<\/jats:italic>\n                      and proteomic evidence supporting the exploration of targeted interventions against parasitic liver disorders.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1919853","type":"journal-article","created":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T04:26:04Z","timestamp":1788841564000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["GHSR and TLR4 collectively promote hepatic inflammation and aberrant repair in alveolar echinococcosis"],"prefix":"10.3389","volume":"17","author":[{"given":"Guangfeng","family":"Chen","sequence":"first","affiliation":[{"name":"The First Affiliated Hospital of Shihezi University","place":["Shihezi, China"]},{"name":"Department of Abdominal 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