This Week In Biofilms And Microbiomes: Monday July 25, 2016

A round-up of what we read last week in the media's coverage of biofilms and microbiomes research.

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Jul 25, 2016
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In a new study, published in the Journal of Bacteriology last week, researchers from the Uniformed Services University, Bethesda, Maryland and Vanderbilt University, Nashville, Tennessee have identified a regulatory protein that controls the formation of biofilms in the ulcer and stomach cancer causing bacteria, Helicobacter pylori. Most bacteria cannot survive in the acidic environment of the human stomach, but H. pylori rapidly respond to the fluctuating conditions and thrive under such circumstances. In the hopes of understanding the mechanism involved in the adoption of the pathogen to stressful environments–like changing levels of acidity, the investigators created a series of H. pylori strains, containing combinations of mutations in three known important regulatory systems - Fur (ferric uptake regulator), NikR (nickel response regulator), and ArsRS (two-component acid response system), which are key to the success of this pathogen. The team was surprised to find that strains lacking ArsS formed large aggregates and a biofilm-like matrix at the air liquid interface of the growth flask. Molecular characterization of biofilm formation showed that strains containing mutations in the ArsRS pathway displayed increased levels of cell aggregation and adherence, both of which are paramount to biofilm development. "Mechanistically, this appears to be due to changes in expression of genes that affect surface adherence and bacterial aggregation," said D. Scott Merrell, Ph.D., study author and Professor of Microbiology and Immunology at the Uniformed Services University, Bethesda, MD. Analysis of isogenic mutant strains that contained all possible single, double and triple regulatory mutations in Fur, NikR and ArsS revealed a previously unrecognized role for the acid responsive two-component system, ArsRS, in biofilm formation. “The research gives us clues about signals that may affect biofilm formation," said Merrell. These avenues may ultimately lead to better control of this pathogen. The study was picked up by NewsWise and Science Daily.

This paper, published in Scientific Reports, suggests that long-term treatment with broad spectrum antibiotics weaken Alzheimer's disease progression through changes in the gut microbiome. Alzheimer’s disease, a progressive neurodegenerative disorder, is characterized by the presence of extracellular aggregates of amyloid-β (Aβ) peptides and intraneuronal neurofibrillary tangles. Neuro-inflammation is also a consistent pathological feature of Alzheimer’s. Buildup of Aß into plaques plays a central role in the onset of Alzheimer's, while the severity of neuro-inflammation is believed to influence the rate of cognitive decline from the disease. Based on the recent body of evidence suggesting a significant role for gut microbes in controlling host immunity and brain function, researchers from the University of Chicago hypothesized that the composition of the intestinal microbiota plays a key role in modulating neuro-inflammation that in turn, influences Aβ deposition. The team administered a cocktail of broad-spectrum antibiotics to mice over a 5-6 month period. Genetic analysis of the gut bacteria from the treated mice showed that while the quantity of microbes present in the gut was similar to the controls’, the diversity of bugs were noticeably different. Instead of hosting a wide variety of bacteria, the antibiotic-treated mice had a less diverse crowd. The mice treated with antibiotics experienced more than a twofold decrease in Aβ plaques than mice that didn’t receive the drugs. Levels of important signaling chemicals circulating in the blood were also elevated in the treated mice. The study concludes that these findings indicate that a chronic, staged antibiotic regimen is able to establish a stable, but altered state of the gut microbiota that is associated with changes in glial and immune functions capable of mitigating Aβ amyloidosis. "We have to find ways to intervene when a patient starts showing clinical signs, and if we learn how changes in gut bacteria affect onset or progression, or how the molecules they produce interact with the nervous system, we could use that to create a new kind of personalized medicine," said Sangram Sisodia, PhD, Thomas Reynolds Sr. Family Professor of Neurosciences at the University of Chicago and senior author of the study. The study was highlighted by several media outlets, including EurekAlert, ScienceNews and Gen News.

We’d love to hear what you’ve been reading this week. Please comment below.

Go to the profile of Richa Dandona

Richa Dandona

Partnerships and Operations Manager, Nature Partner Journals, Nature Research

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