International immunopharmacologyOct 23, 2026

Gut bacteria-produced indole-3-acetic acid may improve teen cognitive problems from severe gut inflammation by reducing brain inflammation and protecting nerve connections

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 24, 2026

Abstract

Gut microbiota-derived indole-3-acetic acid (IAA) may influence cognitive deficits associated with necrotizing enterocolitis (NEC).

Necrotizing enterocolitis (NEC) is linked to cognitive deficits in adolescents.
Gut-brain axis dysfunction may mediate brain injury related to NEC.
The metabolic mechanisms connecting gut microbiota to cognitive impairment are not fully understood.
Indole-3-acetic acid (IAA) could play a role in neuroinflammation and synaptic damage resulting from NEC.
AHR signaling may be involved in the impact of IAA on cognitive dysfunction following NEC.

Simplified

Necrotizing enterocolitis (NEC) is the most severe acute gastrointestinal disease in preterm infants and is an independent risk factor for adolescent-stage cognitive deficits, especially persistent cognitive impairment. Accumulating evidence indicates that gut-brain axis dysfunction mediates NEC-related brain injury. However, the precise metabolic mechanism linking gut microbiota to sustained cognitive deficits remains unclear. This study aimed to explore the effects of gut microbiota-derived indole-3-acetic acid (IAA) and its downstream AHR signaling on NEC-induced neuroinflammation, synaptic damage and cognitive dysfunction.

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Gut bacteria-produced indole-3-acetic acid may improve teen cognitive problems from severe gut inflammation by reducing brain inflammation and protecting nerve connections

Abstract

Full Text

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