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Certain\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Escherichia coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    (\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    ) strains harbour virulence\u2010associated features that promote intestinal colonization, barrier disruption and immune activation. Recent microbiome and metagenomic studies have reported an enrichment of\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    in patients with IgAN, suggesting a potential link to the mucosa\u2013kidney axis. Nevertheless,\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    may contribute to IgAN through two major pathways. First, sustained LPS exposure may induce aberrant production of galactose\u2010deficient IgA1 (Gd\u2010IgA1) by stimulating B cells and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome in macrophages, thereby amplifying systemic and renal inflammation. Second, metabolic reprogramming is associated with increased circulating sphingosine\u20101\u2010phosphate (S1P) and altered production of indole and trimethylamine (TMA); S1P may promote mesangial proliferation and fibrosis, whereas indole\u2010 and TMA\u2010related pathways may contribute to tubulointerstitial injury and chronic kidney disease (CKD) progression. Beyond conventional gut microbiota\u2010targeted interventions, emerging precision therapeutic strategies offer promising new directions for the etiological treatment of IgAN. This review summarizes\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    virulence factors, pathogenesis, and host, environmental, and ecological factors driving its gut expansion in IgAN patients and outlines corresponding therapeutic strategies.\n                  <\/jats:p>","DOI":"10.1111\/1751-7915.70455","type":"journal-article","created":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T09:42:37Z","timestamp":1791798157000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Potential Roles of\n                    <i>Escherichia coli<\/i>\n                    in\n                    <scp>IgA<\/scp>\n                    Nephropathy: Evidence, Mechanistic Hypotheses and Microbiota\u2010Targeted 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