Chronic exposure to stress is associated with increased incidence of depression, generalized anxiety, and PTSD. However, stress induces vulnerability to such disorders only in a sub-population of individuals, as others remain resilient. Inflammation has emerged as a putative mechanism for promoting stress vulnerability.
Using a rodent model of social defeat, we have previously shown that rats with short-defeat latencies (SL/vulnerablerats) show increased anxiety- and depression-like behaviors, and these behaviors are mediated by inflammation in the ventralhippocampus. The other half of socially defeated rats show long-latencies to defeat (LL/resilient) and are similar to controls. Because gut microbiota are important activators of inflammatory substances, we assessed the role of the gutmicrobiome in mediating vulnerability to repeated social defeat stress.
We analyzed the fecal microbiome of control, SL/vulnerable, and LL/resilient rats using shotgun metagenome sequencing and observed increased expression of immune-modulating microbiota, such as Clostridia, in SL/vulnerablerats. We then tested the importance of gut microbiota to the SL/vulnerable phenotype. In otherwise naive rats treated with microbiota from SL/vulnerablerats, there was higher microglial density and IL-1β expression in the vHPC, and higher depression-like behaviors relative to rats that received microbiota from LL/resilient rats, non-stressed control rats, or vehicle-treated rats. However, anxiety-like behavior during social interaction was not altered by transplant of the microbiome of SL/vulnerablerats into non-stressed rats.
Taken together, the results suggest the gutmicrobiome contributes to the depression-like behavior and inflammatoryprocesses in the vHPC of stressvulnerable individuals.
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