{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T06:50:39Z","timestamp":1767855039416,"version":"3.49.0"},"reference-count":84,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T00:00:00Z","timestamp":1762128000000},"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. Cell. Infect. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Myocardial infarction (MI) is a severe cardiovascular condition arising from a sudden reduction or complete cessation of blood supply via the coronary arteries, resulting in localized necrosis of the corresponding myocardial tissue due to persistent ischemia and hypoxia. It is a life-threatening cardiovascular disease with high death rate and poor prognosis due to myocardial necrosis.\n                      <jats:italic>Echinococcus granulosus<\/jats:italic>\n                      hydatid cyst-secreted antigen B (\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB) has been shown to play a critical role in modulating host immune responses. This study aims to investigate whether the\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB subunit 8 (\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2) is able to mitigate inflammation associated with myocardial infarction and therefore reduce the MI caused mortality in a mouse model,. The MI model was established by ligating the left anterior descending (LAD) coronary artery in male C57BL\/6J mice, followed by intraperitoneal administration of recombinant\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB subunit 2 (r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2) to observe its therapeutic effect on MI and related immunological mechanism. To evaluate the role of r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 in macrophage polarization post-MI, mRNA levels of M1 macrophage marker iNOS and M2 marker\n                      <jats:italic>Arg-1<\/jats:italic>\n                      were determined in infarcted regions using RT-qPCR.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , RAW264.7 macrophages were co-incubated with rEgAgB8\/2 and observe whether r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 is able to promote M2 macrophage polarization under inflammation condition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our study in a MI mouse model demonstrated that treatment with r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 significantly improved cardiac function and survival rates from 66.7% to 94.4% within 28 days post MI surgery compared to MI group without treatment. The levels of pro-inflammatory cytokines TNF-\u03b1 and IL-1\u03b2 were significantly reduced in infarcted region in heart tissue and serum, while regulatory cytokines IL-10 and TGF-\u03b2 were increased following r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 treatment associated with reduced expression of M1 macrophage marker iNOS and increased expression of the M2 macrophage marker Arg-1. The treatment of r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 downregulated NLRP3, caspase-1, and IL-1\u03b2 protein levels in infarcted tissues.\n                    <\/jats:p>\n                    <jats:p>\n                      <jats:italic>In vitro<\/jats:italic>\n                      study with macrophage cell line RAW264.7 further demonstrated that co-incubation of r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 with LPS-induced RAW264.7 cells resulted in a decrease in the proportion of CD86\n                      <jats:sup>+<\/jats:sup>\n                      macrophages (M1) and an increase in the proportion of CD206\n                      <jats:sup>+<\/jats:sup>\n                      macrophages (M2) associated with reduced inflammatory cytokines (TNF-\u03b1 and IL-1\u03b2) and increased regulatory cytokines (IL-10 and TGF-\u03b2), which was consistent with the results obtained from the\n                      <jats:italic>in vivo<\/jats:italic>\n                      experiments in a MI mouse model.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These findings reveal that r\n                      <jats:italic>Eg<\/jats:italic>\n                      AgB8\/2 ameliorates MI in mice by promoting macrophage polarization from M1 to M2 phenotypes through inhibition of the NLRP3\/caspase-1\/IL-1\u03b2 signaling pathway, indicating its potential as a therapeutic agent for MI and other inflammation-related diseases.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcimb.2025.1662758","type":"journal-article","created":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T06:23:29Z","timestamp":1762151009000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Echinococcus granulosus antigen B ameliorates myocardial infarction through promoting M2 macrophage polarization"],"prefix":"10.3389","volume":"15","author":[{"given":"Weixiao","family":"Zhang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bingxin","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sai","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xinlong","family":"Xu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qiwang","family":"Jin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chen","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erhe","family":"Gao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bin","family":"Zhan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shili","family":"Wu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rui","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaodi","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2025,11,3]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1260","DOI":"10.1161\/CIRCRESAHA.120.315937","article-title":"Interleukin-1 and the inflammasome as therapeutic targets in cardiovascular disease","volume":"126","author":"Abbate","year":"2020","journal-title":"Circ. 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