Studies in mice have revealed that antibiotics strong enough to kill off gut bacteria can also stop the growth of new brain cells in the hippocampus . It appears that researchers have uncovered an interesting clue as to why this link exists: “a type of white blood cell seems to act as a communicator between the brain, the immune system and the gut .” Once again, research is revealing just how inextricable the gut and brain really are.
The study saw researchers give mice enough antibiotics to almost decimate their gut microbiota. Interestingly, those that lost their healthy gut bacteria where shown to perform worse in memory tests. They also showed a loss of new brain cell creation or neurogenesis in the hippocampus. Here’s where it gets interesting though: the white blood cell link.
“At the same time that the mice experienced memory and neurogenesis loss, the research team detected a lower level of white blood cells (specifically monocytes) marked with Ly6Chi in the brain, blood, and bone marrow. So researchers tested whether it was indeed the Ly6Chi monocytes behind the changes in neurogenesis and memory .”
Follow up studies further investigated the white blood cell link. Lead author, researcher Susanne Asu Wolf said, “For us it was impressive to find these Ly6chi cells that travel from the periphery to the brain, and if there’s something wrong in the microbiome, Ly6chi acts as a communicating cell .” One investigation saw researchers compare untreated mice to mice with healthy gut bacteria levels but low Ly6chi levels for whatever reason. In both cases, mice with low ly6chi levels showed the same memory and neurogenesis insufficiencies .
The researchers did assert that antibiotics are still remarkably useful but noted the adverse effects that can be tied up with prolonged use . Concerningly, “reconstitution with normal gut flora (SPF) did not completely reverse the deficits in neurogenesis unless the mice, also had access to a running wheel or received probiotics .”
Wolf remarked, “We found prolonged antibiotic treatment might impact brain function. But probiotics and exercise can balance brain plasticity and should be considered as a real treatment option .”
She noted her surprise that the fecal transplant option recovered the broad gut bacteria but did not recover neurogenesis. “This might be a hint towards direct effects of antibiotics on neurogenesis without using the detour through the gut,” she remarked before speculating on what their next course of investigation must be .
This provides the latest piece on insight not only into the importance of the gut microbiome, but also the role of human monocytes. While their role in inflammation had long been uncovered, we could be discovering just how important they are in other aspects of human health .
But the major takeaway from this piece of work is that, when the use of antibiotics cannot be avoided, the use of probiotics and exercise becomes even more important. After all, I think we’d all rather a probiotic and a walk in the sun or a quick jog than a faecal transplant. It turns out the jog and the probiotic are even better when it comes to protecting and promoting brain function.
 Staff Writer Cell Press, 2016. “Antibiotics that kill gut bacteria also stop growth of new brain cells.” Cell Reports via Science Daily https://www.sciencedaily.com/releases/2016/05/160519130105.htm retrieved 15 February 17
 Mohle L, Mattei D, Heimesaat M, Bereswill S, Fischer A, Alutis M, French T, Hambardzumyan D, Matzinger P, Dunay I and Wolf S. 2016. LY6Chi monocytes provide a link between antibiotic-induced changes in gut microbiota and adult hippocampal neurogenesis. Cell Press. Voume 15, Issue 9, p1945-1956 31 May 2016, http://www.cell.com/cell-reports/abstract/S2211-1247(16)30518-6?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124716305186%3Fshowall%3Dtrue retrieved 15 February 2017
 Gaidt M, Ebert T, Chauhan D, Schmidt T, Schmid-Burgk J, Rapino F, Robertson A, Cooper M, Graf T and Hornung V. 2016. Human monocytes engage an alternative inflammasome pathway. Immunity. Volume 44, Issue 4, p833-846 http://www.cell.com/immunity/fulltext/S1074-7613(16)00037-6 retrieved 15 February 2017