Dr. Kevin Foster, from the University of Oxford, visited the Center for Evolution and Medicine at Arizona State University last week to talk about competition and sociability among a variety of bacteria, some of which call our guts home. Using humorous descriptions of psychedelic broccoli, tiger and lion fights, and breathing on hornet’s nests, he walked us through the complexity of sociality found in microbes, which ranges from competition among specific bacterial cells to between-species cooperation. Foster used to study social insects, but now he applies his expertise of social behavior (and kin selection) to microbes. While kin selection provides an evolutionary explanation for many complex social behaviors in eukaryotic organisms, it may also be a good model to use in understanding the behavior of genetically similar microbes and how such behavior may affect human health.
The German philosopher, Friedrich Nietzsche, is known for a number of ideas among which a particularly oft-quoted one is, “That which does not kill us makes us stronger” (https://www.goodreads.com/quotes/30-that-which-does-not-kill-us-makes-us-stronger). A recent report in Cell (Fonseca et al., 2015) offers evidence that in the context of infection and immunity, the above aphorism may not be a reliable guide to reality. (more…)
For decades food manufacturers have marketed saccharin, along with other non-caloric artificial sweeteners (NAS), as healthy alternatives to sugar. Artificial sugar substitutes cannot be digested by humans and have been recommended for patients with diabetes and for those trying to lose weight. However, a new report in the journal Nature suggests that NAS are harmful to metabolic health. In this study, saccharin given to mice and to healthy human subjects worsened glucose control compared to sugar, and had the paradoxical effect of increasing blood glucose levels.
Lead investigator Eran Elinov and his colleagues showed that the intestinal microbiota was responsible for the adverse metabolic effects of saccharin. Saccharin increased numbers of Bacteroides bacteria in the gut and also increased the density of bacteria in the Enterobacteriaceae group while decreasing the number of certain beneficial bacteria, such as Akkermansia mucinophila. Remarkably when fecal bacteria from saccharin-fed humans were transferred to germ-free mice, the mice became glucose intolerant, similar to their human donors. Some human subjects were non-responders, maintaining normal metabolism of glucose after exposure to saccharin. Fecal samples from non-responders were inoculated into germ free mice without causing glucose intolerance. These findings indicate a causal role for the microbiota in the impairment of metabolism by artificial sweeteners.
In 2005 Sarkis Mazmanian and colleagues showed that a single polysaccharide from an intestinal commensal, Bacteroides fragilis, could largely correct the subnormal and functionally distorted development of the immune system that occurs in germ-free mice (Mazmanian et al. 2005). More recently they have shown, using three different models of intestinal inflammation, that the same polysaccharide, given by mouth, can turn on crucial immunoregulatory pathways (Mazmanian et al. 2008). In the discussion of the latter paper they state:- (more…)