{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:15:31Z","timestamp":1791396931526,"version":"4.3.3"},"reference-count":54,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2022,10,26]],"date-time":"2022-10-26T00:00:00Z","timestamp":1666742400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2022,10,26]],"date-time":"2022-10-26T00:00:00Z","timestamp":1666742400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81771394"],"award-info":[{"award-number":["81771394"]}],"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":["82171448"],"award-info":[{"award-number":["82171448"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Focal cortical dysplasia type\u00a0IIb (FCDIIb) and tuberous sclerosis complex (TSC) show persistent neuroinflammation, which promotes epileptogenesis and epilepsy progression, suggesting that endogenous resolution of inflammation is inadequate to relieve neuronal network hyperexcitability. To explore the potential roles of formyl peptide receptor 2 (FPR2), which is a key regulator of inflammation resolution, in epilepsy caused by\u00a0FCDIIb and TSC,\u00a0we examined the expression and cellular distribution of FPR2.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>The expression of FPR2 and nuclear factor\u2010\u03baB (NF\u2010\u03baB) signaling pathway was\u00a0examined by real\u2010time PCR, western blots, and analyzed via one\u2010way analysis of variance. The distribution of FPR2 was detected using immunostaining. The expression of resolvin D1 (RvD1, the endogenous ligand of FPR2) was observed via enzyme\u2010linked immunosorbent assay. Pearson's correlation test was used to evaluate the correlation between the expression levels of\u00a0FPR2 and\u00a0RvD1\u00a0and the clinical variants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The expression of FPR2 was significantly lower in FCDIIb (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.0146) and TSC (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.0006) cortical lesions than in controls, as was the expression of RvD1 (FCDIIb:\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.00431; TSC:\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.0439). Weak FPR2 immunoreactivity was observed in dysmorphic neurons (DNs), balloon cells (BCs), and giant cells (GCs) in FCDIIb and TSC tissues. Moreover, FPR2 was mainly distributed in dysplastic neurons; it was sparse in microglia and nearly absent in astrocytes. The NF\u2010\u03baB pathway was significantly activated in patients with FCDIIb and TSC, and the protein level of NF\u2010\u03baB was negatively correlated with the protein level of FPR2 (FCDIIb:\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.00395; TSC:\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.0399). In addition, the protein level of FPR2 was negatively correlated with seizure frequency in FCDIIb (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.0434) and TSC (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.0351) patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In summary, these results showed that the expression and specific distribution of FPR2 may be involved in epilepsy caused by FCDIIb and TSC, indicating that downregulation of FPR2 mediated the dysfunction of neuroinflammation resolution in FCDIIb and TSC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/iid3.706","type":"journal-article","created":{"date-parts":[[2022,10,26]],"date-time":"2022-10-26T05:11:02Z","timestamp":1666761062000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Downregulated formyl peptide receptor 2 expression in the epileptogenic foci of patients with focal cortical dysplasia type IIb and tuberous sclerosis complex"],"prefix":"10.1002","volume":"10","author":[{"given":"Kaixuan","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Epilepsy Research Center of PLA,\u00a0Xinqiao Hospital Army Medical University (Third Military Medical University) Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongke","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Armed Police Hospital of Chongqing Chongqing 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