Can intestinal microbiota and circulating microbial products contribute to pulmonary arterial hypertension?

Research output: Contribution to journalReview articlepeer-review

25 Scopus citations

Abstract

Pulmonary arterial hypertension (PAH) is a fatal disease with a median survival of only 5-7 yr. PAH is characterized by remodeling of the pulmonary vasculature causing reduced pulmonary arterial compliance (PAC) and increased pulmonary vascular resistance (PVR), ultimately resulting in right ventricular failure and death. Better therapies for PAH will require a paradigm shift in our understanding of the early pathophysiology. PAC decreases before there is an increase in the PVR. Unfortunately, present treatment has little effect on PAC. The loss of compliance correlates with extracellular matrix remodeling and fibrosis in the pulmonary vessels, which have been linked to chronic perivascular inflammation and immune dysregulation. However, what initiates the perivascular inflammation and immune dysregulation in PAH is unclear. Alteration of the gut microbiota composition and function underlies the level of immunopathogenic involvement in several diseases, including atherosclerosis, obesity, diabetes mellitus, and depression, among others. In this review, we discuss evidence that raises the possibility of an etiologic role for changes in the gut and circulating microbiome in the initiation of perivascular inflammation in the early pathogenesis of PAH.

Original languageEnglish (US)
Pages (from-to)H1093-H1101
JournalAmerican journal of physiology. Heart and circulatory physiology
Volume317
Issue number5
DOIs
StatePublished - Nov 1 2019

Keywords

  • dysbiosis
  • endotoxin
  • heart failure
  • inflammation
  • short-chain fatty acids

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural
  • Review

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