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. 2024 Oct;33(12):1373-1378.
doi: 10.1177/09612033241274515. Epub 2024 Aug 17.

Gut microbiome composition and intestinal immunity in antiphospholipid syndrome patients versus healthy controls

Valérie Lbi Jansen  1   2   3 , Mark Davids  1 , Dagmar Jm van Mourik  1   2   4 , Johannes Hm Levels  1 , Michiel Coppens  1   2 , Saskia Middeldorp  5 , Max Nieuwdorp  1 , Thijs E van Mens  1   2   3   4
Affiliations

Gut microbiome composition and intestinal immunity in antiphospholipid syndrome patients versus healthy controls

Valérie Lbi Jansen et al. Lupus. 2024 Oct.

Abstract

Introduction: The gut microbiome is recognized as a factor that could potentially contribute to the persistent antibodies of antiphospholipid syndrome (APS). Gut microbial interventions can both induce and mitigate APS in mice. In human APS patients, anti-beta-2-glycoprotein I (β2GP-1) titers correlate with antibody titers against a gut commensal protein homologous to β2GP-1.

Aim: To investigate the effect of the intestinal microenvironment on human APS. Methods We cross-sectionally compared intestinal microbiota composition quantified by shotgun sequencing; fecal short chain fatty acids (SCFAs), bacterial metabolites known to affect autoimmune processes; and fecal calprotectin, an intestinal inflammatory marker, in APS patients and healthy controls.

Results: Neither alpha nor beta diversity of the gut microbiota differed between APS patients (n = 15) and controls (n = 16) and no taxa were differentially abundant. Moreover, fecal SCFAs and fecal calprotectin, did not differ between the groups.

Conclusion: Gut microbiome effects on the APS phenotype are likely not driven by bacterial overabundance, SCFA production or intestinal inflammation.

Keywords: Antiphospholipid syndrome; Autoimmune disease; Gut microbiome; Intestinal microbiome; lupus anticoagulant.

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Conflict of interest statement

Declaration of conflicting interestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: M.C. has received financial support for research from Bayer, CSL Behring, Roche, UniQure, and Novo Nordisk; honoraria for consulting or lecturing from Alexion, Bayer, CSL Behring, Sobi, and Viatris S.M. reports grants from GSK and Aspen; grants and personal fees from Daiichi-Sankyo, Bayer, Pfizer, and Boehringer Ingelheim; and personal fees from Portola/Alexion, AbbVie, Pfizer/Bristol-Meyers Squibb, Norgine, Viatris, and Sanofi, outside of the submitted work. M.N. is scientific advisor of Caelus Health, however this is not relevant for the content of the current paper.

Figures

Figure 1.
Figure 1.
Gut microbiota in APS patients and controls (A) alpha diversity assessed by Shannon index (B) beta diversity: PCoA of between sample Bray-Curtis dissimilarity (C) R. intestinalis DNA methyltransferase gene abundance. APS: antiphospholipid syndrome; PCoA: principal coordinates analysis; R. intestinalis: Roseburia intestinalis.
Figure 2.
Figure 2.
Fecal short chain fatty acids concentrations in µmol/g corrected for differences in wet and dry weight (A) formate (B) butyrate (C) propionate (D) acetate (E) calprotectin levels in μg/g. APS: antiphospholipid syndrome; HC: healthy controls.
See this image and copyright information in PMC

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