This study evaluated the role of dietary oxalate and intestinal oxalate transporters (SLC26A2, SLC26A3, SLC26A6) in IBD pathogenesis, using gene expression analysis, stool oxalate measurement, and dietary intake data from IBD patients and controls, plus mouse models of chemically induced and spontaneous colitis.
SLC26A2 and SLC26A3 were consistently downregulated across IBD subtypes (Crohn's disease and ulcerative colitis), affected tissues (colon and ileum), and mouse colitis models regardless of diet. CD patients had higher stool oxalate despite variable dietary intake; SLC26A6 expression correlated with stricturing disease behavior in CD, and oxalate-supplemented diet worsened disease activity in mice.
Causality between dietary oxalate and mucosal inflammation cannot be established from these observational and chemically induced colitis data. Dietary oxalate intake was variable among CD patients, making it hard to isolate diet as the driver of elevated stool oxalate. Mouse colitis models may not fully replicate human IBD pathophysiology.
Clinicians should be aware that oxalate transporter downregulation in IBD may increase intestinal oxalate accumulation independent of diet, potentially amplifying mucosal inflammation. While routine dietary oxalate restriction in IBD is not yet evidence-based, patients with high disease activity or stricturing CD may warrant closer attention to dietary oxalate load pending future trials.
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