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The most common form is associated with auto\u2010antibodies to leucine\u2010rich glioma\u2010inactivated 1 (LGI1) protein, the presentation of which includes frequent focal seizures. The exact cause of these auto\u2010antibodies remains unknown, but established predispositions include overrepresented human leukocyte antigen (\n                      <jats:italic>HLA<\/jats:italic>\n                      ) alleles. Yet, these\n                      <jats:italic>HLA<\/jats:italic>\n                      alleles are themselves common in the healthy ancestry\u2010matched population. One potential etiological hypothesis is that an environmental trigger, such as the gut microbiome, interacts with a genetically predisposed individual.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To investigate this, we studied 42 patients with LGI1\u2010antibody encephalitis (LGI1\u2010Ab\u2010E) and 27 familial\/environmentally matched controls, and performed metagenomic shotgun sequencing, to describe the compositional and functional differences in the gut microbiome.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We observed that LGI1\u2010Ab\u2010E gut microbiomes exhibited a significant reduction in the ratio of\n                      <jats:italic>Firmicutes<\/jats:italic>\n                      (or Bacillota) and\n                      <jats:italic>Bacteroidetes<\/jats:italic>\n                      phyla, which is associated with the dosage of\n                      <jats:italic>HLA<\/jats:italic>\n                      susceptibility allele count in patients with LGI1\u2010Ab\u2010E. Furthermore, we identified differences in functional gene profiles in the gut microbiome that led to a reduction of neuroinflammatory protective short\u2010chain fatty acids (SCFAs) in LGI1\u2010Ab\u2010E patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>Taken together, our results suggest that a compositional shift in the gut microbiome of LGI1\u2010Ab\u2010E associates with a neuroinflammatory state, possibly through the reduction of SCFA production. Our study highlights the potential of the gut microbiome to explain some of the complex condition and unravel etiological questions. Validation studies with greater sample sizes are recommended.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/epi.18556","type":"journal-article","created":{"date-parts":[[2025,8,6]],"date-time":"2025-08-06T16:29:31Z","timestamp":1754497771000},"page":"4411-4424","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["The gut microbiome associated with\n                    <scp>LGI1<\/scp>\n                    \u2010antibody encephalitis"],"prefix":"10.1111","volume":"66","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5574-4520","authenticated-orcid":false,"given":"Edmund","family":"Gilbert","sequence":"first","affiliation":[{"name":"School of Pharmacy and Biomolecular Sciences Royal College of Surgeons in Ireland  Dublin Ireland"},{"name":"FutureNeuro SFI Research Centre Royal College of Surgeons in Ireland  Dublin 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