Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Jan 7;216(1):41–59. doi: 10.1084/jem.20180794

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2018 Abdel-Haq et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Figure 2. — Gut–brain communication pathways. Communication between the gut microbiota and the CNS encompasses several conduits along neural, enteric, and immune pathways. (A) Proper microglial maturation and behavior is dependent on crosstalk along the gut–brain axis. Information about the state of peripheral inflammation and GI health is received in the CNS via vagal afferents that innervate the GI tract and can influence microglial activation and neuroinflammation. Fine-tuning of the intestinal barrier by gut microbiota and their interactions with gut immune cells modulates peripheral inflammation and can trigger downstream inflammatory responses in the CNS. BBB-permeable bacterial metabolites, including SCFAs, modulate microglial maturation through mechanisms that are yet to be determined. (B) The absence of gut microbes in GF mice confers a variety of physiological abnormalities in neural and microglial behavior in the CNS, resulting in heightened anxiety, stress, hyperactivity, and other behavioral symptoms. BDNF, brain-derived neurotrophic factor; HDAC, histone deacetylase.