{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T02:57:02Z","timestamp":1787021822299,"version":"build-2736575974"},"reference-count":53,"publisher":"Public Library of Science (PLoS)","issue":"2","license":[{"start":{"date-parts":[[2021,2,18]],"date-time":"2021-02-18T00:00:00Z","timestamp":1613606400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["NSFC 31520103916"],"award-info":[{"award-number":["NSFC 31520103916"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31872467"],"award-info":[{"award-number":["31872467"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Key Research and Development Program of China","award":["2017YFD0501300"],"award-info":[{"award-number":["2017YFD0501300"]}]},{"name":"Program for JLU Science and Technology Innovative Research Team and Fundamental Research Funds for the Central Universities, JLU."}],"content-domain":{"domain":["www.plosntds.org"],"crossmark-restriction":false},"short-container-title":["PLoS Negl Trop Dis"],"abstract":"<jats:p>\n                    <jats:italic>Trichinella spiralis<\/jats:italic>\n                    (\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    ) is a widely distributed pathogenic microorganism that causes trichinellosis, a disease that has the potential of causing severe harm to their host. Numerous studies have demonstrated that autophagy can be triggered by microbial infection, such as bacteria, viruses, protozoa, and parasitic helminths. However, it\u2019s still unknown whether autophagy can facilitate host resistance to\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    infection. The present study examined the role of autophagy in striated muscle cell transformation following infection with\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    in BALB\/c mice. Transmission electron microscopy (TEM) was used to detect the production of the host diaphragm autophagosome after\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    infection, and changes in the protein and transcriptional levels of autophagic marker proteins were also detected. The significance of autophagy in\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    infection, namely inhibition of\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    growth, was preliminarily evaluated by conducting\n                    <jats:italic>in vivo<\/jats:italic>\n                    experiments using autophagy inhibitors. Besides, we studied the effect of excretory-secretory products (ES) of\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    on autophagy of C2C12 myoblasts. The changes in protein and gene expression levels in autophagy-related pathways\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    were measured as further evidence. The results showed that\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>spiralis<\/jats:italic>\n                    infection induced autophagy in the host muscle cells. Meanwhile, ES inhibited autophagy of myoblasts\n                    <jats:italic>in vitro<\/jats:italic>\n                    , but this did not affect the cell viability. The upregulation and downregulation of autophagy-related factors in skeletal muscle cells may indicate an adaptive mechanism providing a comfortable niche for the parasite.\n                  <\/jats:p>","DOI":"10.1371\/journal.pntd.0009040","type":"journal-article","created":{"date-parts":[[2021,2,18]],"date-time":"2021-02-18T13:51:09Z","timestamp":1613656269000},"page":"e0009040","update-policy":"https:\/\/doi.org\/10.1371\/journal.pntd.corrections_policy","source":"Crossref","is-referenced-by-count":12,"title":["Effects of Trichinella spiralis and its excretory\/secretory products on autophagy of host muscle cells in vivo and in 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