Microbiota-gut-brain axis
The strangest addition to the wiki’s account of what interoception senses. Every other channel here carries information about the organism’s own state — cardiac, respiratory, gastric, thermal, nociceptive, immune. This one carries information generated by a few trillion organisms that are not the organism, living in its gut, and it reaches the same afferent machinery.
Bonaz et al. (2021) call it “an important channel of interoceptive signaling.” Bonaz’s own research programme is the vagus nerve at the interface of this axis, so the section is written by the person whose claim it is — read accordingly.
The routes
Four, of increasing directness:
- Locally on enteric neurons. Neuroactive compounds produced by intestinal microbiota act on the enteric nervous system in situ.
- Systemic circulation. Microbial-derived signals reach the CNS via the bloodstream — the humoral route, the same door the immune signals of sickness-behaviors come through.
- Via enteroendocrine cells. EECs in the gut epithelium relay luminal signals to vagal afferent fibres; short-chain fatty acids stimulate EECs to release neurotransmitters that activate those afferents. This is the indirect neural route, with the EEC as transducer.
- Directly onto vagal afferents. Bacterial products such as lipopolysaccharides activate toll-like receptors (TLR4) expressed on vagal afferents — bacterial molecules binding receptors on a sensory nerve, with no host cell in between.
Nonvagal pathways also contribute. Alterations in the axis affect subcortical and cortical function, potentially contributing to visceral hypersensitivity and altered pain perception — the proposed bridge to IBS and chronic-pain.
The honest state of the evidence
The review does not oversell this, and the wiki should not either.
Dysbiosis (i.e., abnormal gut microbiota) has been hypothesized as a mechanism involved in IBS, although establishing causality is elusive.
And on treatment: gut dysbiosis has been explored as a therapeutic target in IBS subsets using prebiotics, probiotics, synbiotics and antibiotics, “with generally mixed results” (Ford et al. 2018 meta-analysis). One correlational finding is cited on the imaging side — an association of gut Clostridia with brain functional connectivity and GI sensorimotor function in IBS (Labus et al. 2019, tripartite network analysis) — which is an association in a small literature, not a mechanism.
So: a well-described set of anatomical routes, and a weak set of causal claims about what travels down them and what it does. The gap between “there is a pathway” and “the pathway explains the disorder” is wide here, and this is a field with a considerable popular-science overhang. Recorded as a real interoceptive channel with real receptors, and an open question as to its clinical weight.
Why it matters for the wiki’s concepts
Two consequences worth holding.
It widens what counts as an interoceptive signal. Petzschner et al. propose that interoception and exteroception be distinguished by the type of state being inferred (internal vs external) rather than by sensory channel. The microbiota case pushes on that from the other side: the microbiome is not straightforwardly internal or external — it is neither self nor environment on any tidy definition — and its signals arrive through the canonical interoceptive afferents. The channel-based criterion says interoceptive; the state-based criterion has to decide whose state is being inferred.
It extends the timescale problem. Petzschner et al. catalogue interoceptive signals spanning five orders of magnitude in time, from cardiac (seconds) to immune (weeks). Microbial composition shifts over days to months with diet and antibiotics. Any model that treats interoception as inference over a stationary body has a harder problem than it thinks.