. 2022 Mar 2;22(3):161–170. doi: 10.1007/s11910-022-01179-6

Table 1.

Mechanisms by which infection and gut dysbiosis impact stroke

Condition	Mechanisms for increased stroke risk	Mechanisms for worse stroke outcome
Chronic infection: Periodontal disease	• Chronic inflammation • ↑Atherosclerosis • Initiation and persistence of atrial fibrillation	• Endothelial injury and vascular inflammation • ↑Peri-procedural adverse events
Acute infection: COVID-19	• Immune dysregulation • Direct microvascular injury • Coagulopathy • ↑Acute cardiac injury and arrhythmia	• BBB damage • ↑LVO/stroke severity • ↑Secondary inflammation • Lymphopenia
Gut dysbiosis^*	• Altered ratio of pro-inflammatory T cells (Th1, Th17, γδ IL-17 +) to anti-inflammatory T cells (T_reg) • Decreased levels of SCFA • ↑Intestinal permeability and bacterial translocation

Condition

Mechanisms for increased stroke risk

Mechanisms for worse stroke outcome

Chronic infection: Periodontal disease

• Chronic inflammation

• ↑Atherosclerosis

• Initiation and persistence of atrial fibrillation

• Endothelial injury and vascular inflammation

• ↑Peri-procedural adverse events

Acute infection: COVID-19

• Immune dysregulation

• Direct microvascular injury

• Coagulopathy

• ↑Acute cardiac injury and arrhythmia

• BBB damage

• ↑LVO/stroke severity

• ↑Secondary inflammation

• Lymphopenia

Gut dysbiosis^*

• Altered ratio of pro-inflammatory T cells (Th1, Th17, γδ IL-17 +) to anti-inflammatory T cells (T_reg)

• Decreased levels of SCFA

• ↑Intestinal permeability and bacterial translocation

Abbreviations: BBB, blood brain barrier; LVO, large vessel occlusion; SCFA, short-chain fatty acid

^*Available mechanistic data regarding gut dysbiosis largely apply to both stroke risk and stroke outcomes