To demonstrate reduction of Akkermansia muciniphila in patients with delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH).

SAH is a type of hemorrhagic stroke. DCI is a complication seen in 20-30% of SAH patients 4-21 days after SAH and is a major contributor to morbidity. Excessive systemic inflammation has been associated with DCI, however, the source of the inflammation is poorly understood. The gut-brain axis (GBA) is a bidirectional communication between the gut and the brain which has been implicated in modulation of inflammation in both the peripheral- and the central- nervous system (CNS). A. muciniphila species has been implicated as a key player within the GBA and enrichment has been shown to reduce inflammation in clinical and preclinical models.

Samples were collected from patients with SAH with DCI (n = 7) and without (n = 21). Fecal samples were collected at 3-5 days after admission amplified via Illumina 16Sv4 v1.2 and processed using Illumina MiSeq v2 2x250 v1.8. An amplicon sequence variant table was built using the DADA2 pipeline and differential abundances calculated using the R package DESeq2 package.

Significant decreases in abundance were observed in the genera Akkermansia (Log2Fold Change [FC] -6.66, p 1.76e-5), Prevotella (FC -5.9, p 1.84e-5), Acidaminococcus (FC -5.49, p 1.87e-4), Bifidobacterium (FC -4.91, p 1.87e-4) and significant increases in the genera Alloprevotella (FC 8.06, p 4.32e-16), Clostridiale_vadinBB60_group (FC 8.93, p 4.09e-16), Paraprevotella (FC 6.57, p 3.13e-14), Ruminoclostridum (FC 5.15, p 8.58e-10).

We showed reduced abundance of A. muciniphila during DCI. A. muciniphila has previously been shown to modulate peripheral inflammation. Abundance of A. muciniphila in the gut may dictate the DCI pathophysiology and needs further attention.