ArticleFrontiers in immunology2026
Associations of hereditary angioedema attacks with intestinal permeability and inflammatory cytokines.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Hereditary angioedema (HAE) is characterized by recurrent subcutaneous and submucosal edema. Gastrointestinal involvement is common; however, the role of intestinal barrier dysfunction and its relationship with systemic inflammation in HAE remains poorly understood. Methods: This cross-sectional study included 169 patients with HAE. Circulating markers of intestinal permeability (e.g., lipopolysaccharide [LPS] and fatty acid-binding protein 2 [FABP2]) and inflammatory cytokines (e.g., interleukin [IL]-1β, IL-6, IL-10, and tumor necrosis factor-α) were measured. Associations with edema location and the HAE activity score (HAE-AS) were evaluated through univariate and multivariable regression models. Exploratory mediation and interaction analyses were performed to assess potential relationships among LPS, IL-6, and gastrointestinal edema. Results: Relative to patients without recent gastrointestinal edema, those with recent gastrointestinal edema had significantly higher serum levels of LPS and IL-6 (P = 0.030 and P = 0.031, respectively); FABP2 levels did not significantly differ. Multivariable logistic regression showed that LPS (odds ratio = 3.90, 95% CI: 1.58-10.35, P = 0.004) and IL-6 (odds ratio = 1.15, 95% CI: 1.01-1.31, P = 0.038) were independently associated with recent gastrointestinal edema. No significant mediation or interaction between LPS and IL-6 was observed. Linear regression analysis indicated that LPS was independently associated with HAE-AS (β = 1.499, P = 0.046). Conclusion: Altered intestinal permeability and inflammatory activation, particularly elevated LPS levels, are closely associated with gastrointestinal manifestations and disease activity in HAE. These findings suggest a gut-angioedema axis contributes to phenotype-specific disease expression. IL-6 may reflect concurrent inflammatory activation; the absence of elevated FABP2 suggests that gastrointestinal edema can occur without overt epithelial injury. These results support a role for the gut environment in shaping disease heterogeneity and provide a basis for further mechanistic studies.
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