3e - GUT MICROBIOME, NEUROINFLAMMATION & HYPERTENSION

Question 1

Core concept

Answer 1

CORE CONCEPT
- Article explores gut-brain axis & neuroimmune pathways in pathogenesis of hypertension
- Emphasizes emerging role of gut dysbiosis & chronic low-grade neuroinflammation as non-traditional risk
factors for elevated blood pressure (BP)

Question 2

Key systems & interactions

Answer 2

Table

Question 3

Mechanisms linking gut to hypertension:
- dysbiosis & SCFA disruption
- gut barrier dysfunction
- microglial activation in CNS
- T-cell mediated inflammation

Answer 3

Dysbiosis & SCFA Disruption
- Short-chain fatty acids (SCFAs) like butyrate, acetate regulate BP through vasodilation, anti-inflammatory
effects & sympathetic modulation
- Dysbiosis → ↓ SCFAs → impaired BP regulation

Gut Barrier Dysfunction
- “Leaky gut” → translocation of bacterial LPS (lipopolysaccharides) into circulation → systemic inflammation
→ CNS inflammation

Microglial Activation in CNS
- Activated microglia (brain’s immune cells) release cytokines → damage to neurons in BP-regulating centers
(eX: paraventricular nucleus)
- Central neuroinflammation = sustained sympathetic nervous system activation

T-cell Mediated Inflammation
- Gut dysbiosis triggers differentiation of pro-hypertensive immune cells (Th17, CD8+ T cells)
- These cells migrate to brain & vessels, maintaining chronic inflammation

Question 4

Evidence supporting gut-brain BP axis

Answer 4

• Germ-free mice have lower BP and are resistant to neurogenic hypertension
• FMT (Fecal Microbiota Transplantation) from hypertensive animals induces high BP in normotensive recipients
• Probiotics and SCFA supplementation in animals can lower BP

Question 5

Clinical & therapeutic implications:
- diagnostic considerations
- treatment strategies

Answer 5

Diagnostic Considerations
- Beyond traditional factors: evaluate gut health, inflammatory markers, HR variability & microbial compo
- Potential biomarkers: SCFA levels, LPS, gut-derived cytokines

Table