Residual Endotoxin Activates Dendritic Cells

Over the past few years this newsletter has highlighted several publications indicating the importance of the detection and removal of even sub-clinical levels of endotoxin (e.g., 2013 PLoS One, 2014 JBC). A recent publication from the University of Salzburg further emphasizes this.

Most commercially available recombinant proteins guarantee an endotoxin level less than 1 EU/microgram. The study, published in PLoS One, found that some commercial preps contained more endotoxin than indicated. Additionally, using an array of cytokine assays (IL-6, IL-8, TNFα), NF-κB activation, IL-1β mRNA levels and surface marker expression (CD40, CD80, CD83, CD86) they found that accurately labeled proteins could activate dendritic cells with residual endotoxin levels as low as 0.2 EU/microgram.

BioDtech offers two solutions to the problem of residual endotoxin contamination. First, our EndoBind-R™ technology has been shown to remove even trace amounts of endotoxin. Second, our EndoPrep™ kits can remove interfering proteins to elucidate masked endotoxin not detectable with untreated samples.

Residual Endotoxin Contaminations in Recombinant Proteins are Sufficient to Activate Human CD1c+ Dendritic Cells

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Microbial Zip Codes

A recent report, published by the American Society of Microbiology in the journal mSystems, indicates that specific cities have their own individual microbial fingerprint. Scientists from Northern Arizona University collected microbial samples in three unique building types in three different North American cities (Flagstaff, San Diego, Toronto) over the course of one year. Their findings revealed that parameters such as building size, ventilation, traffic, humidity and heat had little effect on bacterial make-up between buildings in the same city. However, they found clear differences between cities with each city having a unique diversity and mixture of specific microbial species. Additionally, they found that floors contain the most number of microbes and that a significant, but not majority, amount of the microbes come from human skin.

Cities Have Unique Microbial Signatures, Study Shows

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Plastic-Eating Bacteria

The increased use of plastic materials over the past decade has resulted in 311 million tons of plastic waste annually. One of the most significant sources is polyethylene terephalate (PET), the material in disposable water bottles. Recently a group of Japanese scientists began to collect and analyze environmental samples from the property of a PET bottle-recycling factory. They found a new species of bacteria, Ideonella sakaiensis, that was able to convert PET into terephtalic acid and ethylene glycol and digest both. This discovery is remarkable for two reasons. First, since PET was just invented in the 1940’s it shows the tremendous power of evolution. Second, it provides a potential path to address the serious problem of plastic waste.

Bacteria found to eat PET plastics could help do the recycling

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Bacterial Exposure Can Promote Type 2 Diabetes

A recent study has demonstrated a link between bacterial exposure and the development of diabetes mellitus type 2 (DMII). This important work could lead to new treatments or even prevention through species-specific interventions.

Staphylococcus aureus is an opportunistic bacteria that lives on the skin. Colonization by S. aureus is associated with expression of a superantigen called toxic shock syndrome toxin-1 (TSST-1) which results in systemic immune activation. Importantly, there is a positive correlation between obesity and S. aureus colonization. In a recent study using a rabbit model, scientists from the University of Iowa showed that S. aureus colonization, and the resulting TSST-1 exposure, results in a loss in glucose response, increased insulin production, systemic inflammation, liver damage and increased circulating endotoxin – all hallmarks of DMII. To validate these findings they measured TSST-1 levels in DMII patients and found elevated levels. This is the first direct connection between bacterial exposure and diabetes.

Chronic superantigen exposure induces systemic inflammation, elevated bloodstream endotoxin, and abnormal glucose tolerance in rabbits: possible role in diabetes

Diabetes
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Bacteria Communicate Like Brain Cells

Recent work, published in Nature, demonstrates that bacterial cells communicate with each other using ions and ion channels, much like brain cells. In fact, the proteins that form bacterial ion channels are homologous to those in plants and animals. This provides compelling evidence for how individual bacterial cells work in concert to form biofilms. This also provides a new mechanism for antibiotics: dispersing bacteria instead of killing them. This would lead to less bacterial resistance and prevent the destruction of healthy commensal species.

Bacteria Can Communicate Like Brain Cells

Ion channel

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Personalized Diets for Your Gut Bacteria

Research over the past few years has clarified the importance of our individualized gut microbiome in disease and overall health. This observation led scientists from Tel Aviv to monitor food intake, blood-glucose levels and microbiome composition in 1000 patients over the course of 50,000 meals. They found that different individuals tolerated food differently, including some people who could process “unhealthy” foods with ease. Using this data they tailored diets to pre-diabetic patients based on microbiome composition and observed a decrease in blood-glucose spikes. This concept could lead to individualized, or at lease “grouped”, diets.

The Future of Dieting is Personalized Algorithms Based on Your Gut Bacteria

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A Link Between Endotoxin and Obesity

Using both mice and human models, scientists in China have connected endotoxin to obesity. In mice, they found that inflammation associated with low-dosage endotoxin injections led to insulin resistance, weight gain and diabetes. In humans, they identified high levels of endotoxic Enterobacter cloacae B29 in obese patients. Altering the diet specifically to reduce this population of bacteria led to weight loss, decreased inflammation and, in some cases, recovery from diabetes and hypertension.

Weight Loss Via Gut Bacteria: The Microbiome-Obestiy Connection

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Probiotics Reduce HIV-Associated Inflammation

HIV infection causes dysregulation of intestinal microbiota and leads to bacterial translocation of endotoxin into circulation, leading to immune activation and inflammation. Though anti-retroviral therapy (ART) reduces these events, it does not completely normalize gastrointestinal integrity. The extent of intestinal damage and the subsequent immune reaction have been linked to mortality in HIV. In a recent publication in PLoS One, scientists supplemented ART with probiotics and found significant reductions in the levels of immune activation markers, some to a level comparable with healthy controls. These results suggest that it may be possible to significantly improve prognosis in HIV patients with simple maintenance of the microbiota, such as probiotic supplementation and diet change.

Probiotics Reduce Inflammation in Antiretroviral Treated HIV-Infected Individuals: Results of the “Probio-HIV” Clinical Trial

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The Microbiome’s Tipping Point

Every individual’s microbiome is unique and dependent on factors such as genetics and diet. Changes in the relative amounts of each species can alter host health and contribute to various diseases. In a recent Nature Communications publication, scientists show that many bacterial species can shift between stable low- or high-abundance states while intermediate states are unstable and rare. For translational science, this provides the possibility that certain diseases are defined by specific combinations of low/high levels of specific species of bacteria. Understanding these patterns could allow treatments to complicated diseases through intervention at the microbiome level.

The Microbiome’s Tipping Point

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A Bacterial “Back-Up Plan”

Type I Signal Peptidase (SPase) is a bacterial protein that, until recently, was thought to be essential. Because of its key role it has been the target of much antibiotic development. A recent publication by scientists from The Scripps Institute has shown that bacteria have a “back-up plan” if SPase is inhibited. This back-up plan was previously unknown and can turn itself on when it senses that SPase is not adequately functioning. This work underscores the complications in developing effective antibiotics and the hazards of their overuse.

Bacteria Use a Back-Up Plan to Evade Antibiotics

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