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Cell Host Microbe ; 29(1): 83-93.e3, 2021 01 13.
Artigo em Inglês | MEDLINE | ID: mdl-33385335

RESUMO

The immunopathogenesis of inflammatory bowel disease (IBD) has been attributed to a combination of host genetics and intestinal dysbiosis. Previous work in a small cohort of IBD patients suggested that pro-inflammatory bacterial taxa are highly coated with secretory immunoglobulin IgA. Using bacterial fluorescence-activated cell sorting coupled with 16S rRNA gene sequencing (IgA-SEQ), we profiled IgA coating of intestinal microbiota in a large cohort of IBD patients and identified bacteria associated with disease and treatment. Forty-three bacterial taxa displayed significantly higher IgA coating in IBD compared with controls, including 8 taxa exhibiting differential IgA coating but similar relative abundance. Patients treated with anti-TNF-α therapies exhibited dramatically altered microbiota-specific IgA responses compared with controls. Furthermore, increased IgA coating of Oscillospira was associated with a delay in time to surgery. These results demonstrate that investigating IgA responses to microbiota can uncover potential disease-modifying taxa and reveal improved biomarkers of clinical course in IBD.


Assuntos
Bactérias/imunologia , Microbioma Gastrointestinal/imunologia , Microbioma Gastrointestinal/fisiologia , Imunoglobulina A Secretora/imunologia , Doenças Inflamatórias Intestinais/imunologia , Doenças Inflamatórias Intestinais/microbiologia , Adulto , Bactérias/crescimento & desenvolvimento , Clostridiales/crescimento & desenvolvimento , Clostridiales/imunologia , Estudos de Coortes , Colite Ulcerativa/tratamento farmacológico , Colite Ulcerativa/imunologia , Colite Ulcerativa/microbiologia , Colite Ulcerativa/fisiopatologia , Doença de Crohn/tratamento farmacológico , Doença de Crohn/imunologia , Doença de Crohn/microbiologia , Doença de Crohn/fisiopatologia , Progressão da Doença , Feminino , Humanos , Doenças Inflamatórias Intestinais/tratamento farmacológico , Doenças Inflamatórias Intestinais/fisiopatologia , Masculino , Fator de Necrose Tumoral alfa/antagonistas & inibidores
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