Microbiota Communication


I found that both papers brought valuable insight to our understanding of the gut-brain axis. Reber et. al showed that administration of heated Mycobacterium Vaccae induced behavioral changes associated with decreased stress response, measured by EPM, and linked these findings with associated prevention of stress induced decrease of slc6a4 and tph2 mRNA expression in the dorsal raphe nucleus (seretonin bioavailability), as well as preventive effects in colon tissue damage in acute colitis. Since glucocorticoids have been shown to increase bacterial adhesion and transition into lymph nodes, the mitigation of stress induced inflammatory changes in the gut by M. Vaccae make it a potent target for therapeutic modulation of pathobionts.

I hypothesize that the presence of this probiotic induces anti-inflammatory effects not only via TGF-B signaling and Il-10 cytokine release, but also direct microbiota to microbiota communication mechanisms preventing aggravation of potential pathobionts and relegation of aggravated pathobionts to a non-aggravated state. Thus further research on not only cross talk between microbiota with immune receptors but also direct communication among microbiota may prove valuable.

That MRHD offspring mice would exhibit a reduction in NMDAr mediated LTP in the mesolimbic (VTA) pathway as well as a reduction in oxytocin producing cells in the PVN of the hypothalamus is illuminating since it shows a potential pathway in which a HFD can induce negative changes in social communication both via oxytocin bioavailability, and hedonic response to social interaction with a novel litter mate.

I found it wholly interesting that M. Vaccae increased Iba1-stained microglia in the medial prefrontal cortex which are centers for anxiety and fear. I hypothesize that activation of microglia induces clearance of cell debris and toxic by products of inflammation which, left circulating, could induce a positive feedback loop of an anxiogenic inflammatory signaling pathway.

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