In the topic of gut microbiota, the researchers Reber et al investigated numerous approaches to the effect that bacteria M. vaccae has on stress, colitis and anxiety behavior in mice. It was intriguing to read that there was a larger likelihood of stress-related disorders for people in countries with a diet low in microbiota, exposure to few old infected pathogens, and few organisms from the natural environment. It is expected that vulnerability to these factors would create an inflammatory response in the body, but instead, the lack of exposure increases the prevalence of stress disorders. As stress is a large umbrella term, I would like to see more research by these researchers specifically of how mineralocorticoid receptors for acute, pro-inflammatory activity would affect stress. A comparison/contrasting of this to the effect that glucocorticoid receptors (responsible for high and chronic stress exposure) would have may enable a deeper understanding of the topic. The relation of these two stress-responsive receptors to the bacterium M. vaccae could also be a suggestive future investigative measure.
The overall structure of the paper was not as clear as the second paper by Buffington et al. For example, more clarity in labelling the figures to the respective experiments and potentially including more supplemental figures in the paper itself would enable a better understanding of the intentions. Perhaps this was not a possibility due to formatting restrictions of the journal. Despite this, the paper provided deep insight to the effect of gut microbiome and multiple approaches to the relation between the risk of inflammation and stress pathology. Applying the mice findings to humans would aid the expansion of immunization and diseases such as IBS, which are painful to experience in patients, and thereby provide potential ideas for treatment.
In the paper by Buffington et al in 2016, the role of gut microbes and the relation to maternal high fat diet and social behavior was investigated. I was interested to read about a hormone that we have not yet talked about in class, oxytocin, and the influence that it has on social behavior. I also learned about the large effect that the gut-brain axis has on behavioral responses, specifically in neuropsychiatric disorders. A few weeks ago in one of my other courses, we were taught that mice with autism spectrum disorder (ASD) tend to be defined with deficits in social interactions and communication. Thus, in a study by Dinan et al, animal models of social behaviors were tested. It was found that animals with ASD preferred to interact with a novel object rather than a conspecific and a familiar mouse rather than a novel mouse. These results are opposite to that of non-autistic mice’s preferences. The findings align well with the first section of the paper which suggests that MHFD offspring which are more likely to have ASD appear to be socially impared. Reading this paper also reminded me of the evidence that re-colonization with fecal samples from non-germ free mice to that of germ free mice would result in a change in their cognitive activity, indicating the strong effect of the gut-brain axis. Buffington and colleagues mention that co-host family members are known to share similar microbiota. Does this therefore mean that paternal or sibling microbiota in addition to maternal microbiota can be the same as that of the offspring? Is there any present research suggesting such a relationship? Additionally, I would be interested in knowing more about the researcher’s future directions as they only briefly mention this in the discussion. For example, whether they would be interested in conducting future studies on other roles that oxytocin have, or other neuropsychiatric disorders or diseases (such as diabetes) that affect offspring on the basis of maternal obesity.
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