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We previously demonstrated enrichment in sulfidogenic microbes in quiescent Crohn\u2019s disease patients with (qCD\u2005+\u2005S) vs without persistent GI symptoms (qCD-S). Thus, we hypothesized that sulfur metabolic pathways would be enriched in stool while differentially abundant microbes would be associated with important sulfur metabolic pathways in qCD\u2005+\u2005S.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed a multicenter observational study nested within SPARC IBD. Quiescent inflammation was defined by fecal calprotectin level\u2005&amp;lt;\u2005150 mcg\/g. Persistent symptoms were defined by CD-PRO2. Active CD (aCD) and non-IBD diarrhea-predominant irritable bowel syndrome (IBS-D) were included as controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Thirty-nine patients with qCD\u2005+\u2005S, 274 qCD-S, 21 aCD, and 40 IBS-D underwent paired shotgun metagenomic sequencing and untargeted metabolomic profiling. The fecal metabolome in qCD\u2005+\u2005S was significantly different relative to qCD-S and IBS-D but not aCD. Patients with qCD\u2005+\u2005S were enriched in sulfur-containing amino acid pathways, including cysteine and methionine, as well as serine, glycine, and threonine. Glutathione and nicotinate\/nicotinamide pathways were also enriched in qCD\u2005+\u2005S relative to qCD-S, suggestive of mitochondrial dysfunction, a downstream target of H2S signaling. Multi-omic integration demonstrated that enriched microbes in qCD\u2005+\u2005S were associated with important sulfur metabolic pathways. Bacterial sulfur metabolic genes, including CTH, isfD, sarD, and asrC, were dysregulated in qCD\u2005+\u2005S. Finally, sulfur metabolites with and without sulfidogenic microbes showed good accuracy in predicting the presence of qCD\u2005+\u2005S.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Microbial-derived sulfur pathways and downstream mitochondrial function are perturbed in qCD\u2005+\u2005S, which implicate H2S signaling in the pathogenesis of this condition. Future studies will determine whether targeting H2S pathways results in improved quality of life in qCD\u2005+\u2005S.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ibd\/izae238","type":"journal-article","created":{"date-parts":[[2024,9,19]],"date-time":"2024-09-19T15:29:09Z","timestamp":1726759749000},"page":"763-776","source":"Crossref","is-referenced-by-count":4,"title":["Why Symptoms Linger in Quiescent Crohn\u2019s Disease: Investigating the Impact of Sulfidogenic Microbes and Sulfur Metabolic Pathways"],"prefix":"10.1093","volume":"31","author":[{"given":"Jonathan","family":"Golob","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, University of Michigan , Ann Arbor, MI ,","place":["USA"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Krishna","family":"Rao","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, University of Michigan 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