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The mechanisms underlying this phenomenon, termed central trained immunity, remain poorly understood. We hypothesized that infection induces histone modifications leading to changes in chromatin accessibility that are conserved during differentiation from HSPCs to myeloid progenitors and monocytes. We conducted genome-wide surveillance of histone marks H3K27ac and H3K4me3 and chromatin accessibility in hematopoietic stem cells, multipotent progenitor 3, granulocyte-monocyte progenitors, and monocytes and macrophages of naive and\n                    <jats:italic>Mycobacterium avium<\/jats:italic>\n                    \u2013infected mice. IFN signaling pathways and related transcription factor binding motifs including IRFs, NF-\u03baB, and CEBP showed increased activating histone marks and chromatin accessibility across cell types. However, histone marks and increased chromatin accessibility were conserved at only a few loci, notably\n                    <jats:italic>Irf1<\/jats:italic>\n                    and\n                    <jats:italic>Gbp6<\/jats:italic>\n                    . Knock out of\n                    <jats:italic>IRF1<\/jats:italic>\n                    disrupted enhanced mitochondrial respiration and bacterial killing in human monocyte cell lines, while\n                    <jats:italic>GBP6-<\/jats:italic>\n                    KO monocyte cell lines showed dysregulated mitochondrial respiration. In summary, this study identifies IRF1 and GBP6 as 2 key loci at which infection-induced systemic inflammation leads to epigenetic changes that are conserved from HSPCs to downstream monocytes, providing a mechanistic avenue for central trained immunity.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.193686","type":"journal-article","created":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T17:00:25Z","timestamp":1765299625000},"source":"Crossref","is-referenced-by-count":4,"title":["Rare epigenetic alterations are conserved across hematopoietic differentiation stages after mycobacterial infection"],"prefix":"10.1172","volume":"11","author":[{"given":"Brandon T.","family":"Tran","sequence":"first","affiliation":[{"name":"Graduate Program in Cancer and Cell Biology,"},{"name":"Department of Pediatrics, Division of Infectious Disease, Texas Children\u2019s Hospital and Baylor College of Medicine,"},{"name":"Stem Cells and Regenerative Medicine Center,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pamela N.","family":"Luna","sequence":"additional","affiliation":[{"name":"Department of Molecular and Human Genetics,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruoqiong","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Texas Children\u2019s Hospital and Baylor College of Medicine,"},{"name":"Stem Cells and Regenerative Medicine Center,"},{"name":"Graduate Program in Immunology and Microbiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Duy T.","family":"Le","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Texas Children\u2019s Hospital and Baylor College of Medicine,"},{"name":"Stem Cells and Regenerative Medicine Center,"},{"name":"Graduate Program in Immunology and Microbiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Apoorva","family":"Thatavarty","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Texas Children\u2019s Hospital and Baylor College of Medicine,"},{"name":"Stem Cells and Regenerative Medicine Center,"},{"name":"Graduate Program in Molecular and Human Genetics,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laure","family":"Maneix","sequence":"additional","affiliation":[{"name":"Stem Cells and Regenerative Medicine Center,"},{"name":"Huffington Center of Aging, and"},{"name":"Dan L. 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