{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T19:19:58Z","timestamp":1791400798046,"version":"4.3.3"},"reference-count":52,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,12,19]],"date-time":"2024-12-19T00:00:00Z","timestamp":1734566400000},"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><jats:title>Introduction<\/jats:title><jats:p>AE and whether the inhibition of the MyD88 inflammatory pathway can enhance Ghrelin expression to collaboratively modulate AE progression remains unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In this study, we evaluated Ghrelin serum levels and changes in TLR4\/MyD88\/NF-\u03baB pathway proteins and inflammatory factors in AE patients and <jats:italic>E. multilocularis<\/jats:italic> mouse models at different stages of infection (-4, -8, and -12 weeks). Additionally, we administered the MyD88 inhibitor TJ-M2010-5 intraperitoneally to infected mice to evaluate alterations in inflammation and Ghrelin levels, as well as disease progression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A decrease in serum Ghrelin levels in AE patients, whereas both Ghrelin and GHSR, along with TLR4\/MyD88\/NF-\u03baB pathway proteins and markers of M1\/M2 macrophage polarization, exhibited increased expression in the inflammatory cell zones surrounding hepatic lesions. Similar findings were observed in <jats:italic>E.\u00a0multilocularis<\/jats:italic>-infected mice. M1-type inflammatory expression predominated throughout the infection\u2019s progression, with sustained high levels of Ghrelin counteracting inflammation. The TLR4\/ MyD88\/NF-\u03baB pathway remained suppressed during the first 8 weeks, becoming activated only at 12\u00a0weeks. Inhibition of the MyD88 pathway resulted in reduced inflammation levels and upregulated Ghrelin expression, thereby collaboratively regulating the progression of hepatic infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings suggest an interactive regulation between the MyD88 inflammatory signaling pathway and Ghrelin, indicating that MyD88 inhibition could enhance Ghrelin expression to modulate the progression of <jats:italic>E.\u00a0multilocularis<\/jats:italic> infection.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fimmu.2024.1512180","type":"journal-article","created":{"date-parts":[[2024,12,19]],"date-time":"2024-12-19T05:10:22Z","timestamp":1734585022000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Inhibition of the MyD88 signaling pathway could upregulates Ghrelin expression to synergistically regulate hepatic Echinococcus multilocularis-infected 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