钙蛋白酶
微生物群
肠道菌群
免疫学
粪便
抗磷脂综合征
抗体
免疫
医学
生物
炎症性肠病
微生物学
免疫系统
疾病
内科学
生物信息学
作者
van Noorle Jansen,Mark Davids,Dagmar JM van Mourik,Johannes H.M. Levels,Michiel Coppens,Saskia Middeldorp,Max Nieuwdorp,Thijs E. van Mens
出处
期刊:Lupus
[SAGE]
日期:2024-08-17
标识
DOI:10.1177/09612033241274515
摘要
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.
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