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Pulmonary Arterial Hypertension Patients Have a Proinflammatory Gut Microbiome and Altered Circulating Microbial Metabolites.
Moutsoglou, Daphne M; Tatah, Jasmine; Prisco, Sasha Z; Prins, Kurt W; Staley, Christopher; Lopez, Sharon; Blake, Madelyn; Teigen, Levi; Kazmirczak, Felipe; Weir, E Kenneth; Kabage, Amanda J; Guan, Weihua; Khoruts, Alexander; Thenappan, Thenappan.
Afiliação
  • Moutsoglou DM; Division of Gastroenterology, Hepatology, and Nutrition.
  • Tatah J; Division of Cardiovascular Medicine, Department of Medicine.
  • Prisco SZ; Division of Cardiovascular Medicine, Department of Medicine.
  • Prins KW; Division of Cardiovascular Medicine, Department of Medicine.
  • Staley C; Division of Basic and Translational Research, Department of Surgery, and.
  • Lopez S; Division of Gastroenterology, Hepatology, and Nutrition.
  • Blake M; Division of Cardiovascular Medicine, Department of Medicine.
  • Teigen L; Division of Gastroenterology, Hepatology, and Nutrition.
  • Kazmirczak F; Division of Cardiovascular Medicine, Department of Medicine.
  • Weir EK; Division of Cardiovascular Medicine, Department of Medicine.
  • Kabage AJ; Division of Gastroenterology, Hepatology, and Nutrition.
  • Guan W; Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota.
  • Khoruts A; Division of Gastroenterology, Hepatology, and Nutrition.
  • Thenappan T; Division of Cardiovascular Medicine, Department of Medicine.
Am J Respir Crit Care Med ; 207(6): 740-756, 2023 03 15.
Article em En | MEDLINE | ID: mdl-36343281
ABSTRACT
Rationale Inflammation drives pulmonary arterial hypertension (PAH). Gut dysbiosis causes immune dysregulation and systemic inflammation by altering circulating microbial metabolites; however, little is known about gut dysbiosis and microbial metabolites in PAH.

Objectives:

To characterize the gut microbiome and microbial metabolites in patients with PAH.

Methods:

We performed 16S ribosomal RNA gene and shotgun metagenomics sequencing on stool from patients with PAH, family control subjects, and healthy control subjects. We measured markers of inflammation, gut permeability, and microbial metabolites in plasma from patients with PAH, family control subjects, and healthy control subjects. Measurements and Main

Results:

The gut microbiome was less diverse in patients with PAH. Shannon diversity index correlated with measures of pulmonary vascular disease but not with right ventricular function. Patients with PAH had a distinct gut microbial signature at the phylogenetic level, with fewer copies of gut microbial genes that produce antiinflammatory short-chain fatty acids (SCFAs) and secondary bile acids and lower relative abundances of species encoding these genes. Consistent with the gut microbial changes, patients with PAH had relatively lower plasma concentrations of SCFAs and secondary bile acids. Patients with PAH also had enrichment of species with the microbial genes that encoded the proinflammatory microbial metabolite trimethylamine. The changes in the gut microbiome and circulating microbial metabolites between patients with PAH and family control subjects were not as substantial as the differences between patients with PAH and healthy control subjects.

Conclusions:

Patients with PAH have proinflammatory gut dysbiosis, in which lower circulating SCFAs and secondary bile acids may facilitate pulmonary vascular disease. These findings support investigating modulation of the gut microbiome as a potential treatment for PAH.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Vasculares / Microbioma Gastrointestinal / Hipertensão Arterial Pulmonar Limite: Humans Idioma: En Revista: Am J Respir Crit Care Med Assunto da revista: TERAPIA INTENSIVA Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Vasculares / Microbioma Gastrointestinal / Hipertensão Arterial Pulmonar Limite: Humans Idioma: En Revista: Am J Respir Crit Care Med Assunto da revista: TERAPIA INTENSIVA Ano de publicação: 2023 Tipo de documento: Article