GIT

[Jo Bowyer]

Cellular tango: Immune and nerve cells work together to fight gut infections

https://www.sciencedaily.com/release...0907112416.htm

The study, published Sept. 6 in Nature, shows that the immune system and nervous system have co-evolved to respond to infectious threats. This means that scientists looking for ways to treat diseases like inflammatory bowel disease or asthma that involve an excessive immune system response may also have to address the nervous system's role.

"The immune system and neuronal system don't act independently," said senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease and the Michael Kors Professor of Immunology at Weill Cornell Medicine. "They are working together."

"These guys are dancing like a tango," Dr. Klose said. The lining of the gut is home to many immune system cells, which serve as a defense against parasites and other infections. It is also loaded with nerve cells. Lead author Dr. Christoph Klose, a postdoctoral associate at the Roberts Institute, found that immune system cells in the gut, called group 2 innate lymphoid cells (ILC2s), are intertwined with nerve cells called cholinergic neurons.

The cells' close proximity led the researchers to wonder if they may be communicating. That's when they discovered that the ILC2 cells had a receptor for a protein called neuromedin U (NMU), which acts as a messenger for the nerve cells. In laboratory experiments, the investigators found that exposing ILC2 cells to NMU causes the ILC2 cells to rapidly multiply and secrete chemicals called cytokines that may help trigger an immune response or cause inflammation.

My bold FYI ectodermalists.

[Jo Bowyer]

Chemotherapy, pain, and gut microbiota

http://stke.sciencemag.org/content/10/496/eaap9098.full

[Jo Bowyer]

BLOCKING GUT BACTERIA STRAINS MAY REDUCE AUTISM RISK LINKED TO MATERNAL INFECTION

http://neurosciencenews.com/infectio...y-autism-7479/

Mothers who experience an infection severe enough to require hospitalization during pregnancy are at higher risk of having a child with autism. Two new studies from MIT and the University of Massachusetts Medical School shed more light on this phenomenon and identify possible approaches to preventing it.

My mother had to have her appendix removed seven months in to her pregnancy with me. Although high functioning autism has given me huge advantages in life, not least an ability to interact with patients on the spectrum, I did everything to avoid predisposing factors while I was pregnant. My daughter is neurotypical.

[Jo Bowyer]

Stress May Be Just As Unhealthy As Junk Food To Digestive System

http://neurosciencenews.com/stress-d...e-system-7747/

Summary:

Stress causes gut microbiota composition to shift as though a female mouse is on a high fat diet, researchers report.

[Jo Bowyer]

Low-complexity microbiota in the duodenum of children with newly diagnosed ulcerative colitis


http://journals.plos.org/plosone/art...l.pone.0186178


Abstract

Background


Inflammatory bowel disease (IBD) is characterized by gut dysbiosis. To date, the large bowel microbiota has been in focus. However, the microbiota of the small intestine may also be of importance, as the small bowel is a site for the induction and control of mucosal immune responses, which can be modulated by constituents of the local microbiota.

Methods


Duodenal fluids were collected during diagnostic work-up of treatment-naïve children who were suspected of having IBD. The duodenal fluids were analyzed by pyrosequencing (average of 32,000 reads/sample, read length of 500 nucleotides). After diagnosis, the duodenal microbiota of subjects with ulcerative colitis (N = 8) or Crohn’s disease (N = 5), and non-IBD controls (N = 8) were compared.

Results


Pyrosequencing revealed that the duodenal microbiota of children with ulcerative colitis contained fewer Operational Taxonomic Units (OTUs) per individual than the duodenal microbiota of the controls (P = 0.005). This reduction in richness of the duodenal microbiota was seen for three major phyla: Firmicutes, Actinobacteria, and Bacteroidetes. Several bacterial genera were detected less frequently in the children with ulcerative colitis than in the non-IBD controls, including Collinsella (P = 0.001), Lactobacillus (P = 0.007), and Bacillus (P = 0.007), as well as a non-identified member of the order Sphingobacteriales (P = 0.007).

Conclusions


In this pilot study, we show that the duodenal microbiota of children with ulcerative colitis exhibits reduced overall richness, despite the fact that the inflammation is primarily localized to the colon. These results should be corroborated in a larger study.

[Jo Bowyer]

Bacteria have a sense of touch

https://www.sciencedaily.com/release...1026142320.htm

Although bacteria have no sensory organs in the classical sense, they are still masters in perceiving their environment. A research group has now discovered that bacteria not only respond to chemical signals, but also possess a sense of touch. The researchers demonstrate how bacteria recognize surfaces and respond to this mechanical stimulus within seconds. This mechanism is also used by pathogens to colonize and attack their host cells.

[Jo Bowyer]

No Pain, No Gain: Commensal Bacteria Help Chemotherapy Through Painful Side Effects

http://knowingneurons.com/2017/11/08...EMAIL_CAMPAIGN)

Interestingly, Mao and colleagues at the Massachusetts General Hospital, MA, have recently pointed out that gut bacteria, beyond their significance in the treatment of cancers, also plays a key role in the development of pain after chemotherapy. In the absence of gut bacteria, Oxaliplatin is ineffective in stimulating the necessary inflammatory response required to manifest its tumor-killing properties. Gut bacteria is thus needed to permit the immune cells to mount an inflammatory response. This permissive signal, in the form of a bacterial cell wall component referred to as LPS, is sensed by a specific receptor, which then activates the underlying pain signals in the spinal cord, leading to the painful side effects. Therefore, commensal bacteria enable immune cells to manifest the inflammatory response required for cancer therapy and do so in a painful manner. In other words, exacerbating pain seems to be unavoidable when gut bacteria demonstrate their protective effects against cancers.

Gut bacteria seems to be more than just a normal flora in our bodies. Recent advances in our knowledge suggest that these bacteria are an integral part of different mechanisms with far-reaching effects. The significant role of gut bacteria in the perception of pain after chemotherapy opens up a new avenue for more comprehensive pain and cancer research, aiming to develop more efficient cancer therapies with minimal side effects.

[Jo Bowyer]

Engineering the gut microbiome with 'good' bacteria may help treat Crohn's disease

https://www.sciencedaily.com/release...1115144142.htm

"Because it's a single enzyme that is involved in this process, it might be a targetable solution," said the study's senior author, Gary D. Wu, MD, associate chief for research in the division of Gastroenterology at the Perelman School of Medicine at the University of Pennsylvania. "The idea would be that we could 'engineer' the composition of the microbiota in some way that lacks this particular one."

An imbalance in the gut microbiome -- more "bad" bacteria than "good" -- is known as dysbiosis, which is caused by environmental stressors, such as intestinal inflammation, antibiotics, or diet. Gut dysbiosis is believed to fuel Crohn's disease and other diseases, but the mechanisms behind that relationship is not fully understood by researchers looking to strike a healthier, bacterial balance for patients. Crohn's disease is an inflammatory bowel disease that affects nearly one million children and adults in the United States.

In a series of human and mouse studies, the researchers discovered that a type of "bad" bacteria known as Proteobacteria feeding on urea, a waste product that can end up back in the colon, played an important role in the development of dysbiosis.

The "bad" bacteria, which harbor the urease enzyme, convert urea into ammonia (nitrogen metabolism), which is then reabsorbed by bacteria to make amino acids that are associated with dysbiosis in Crohn's disease. "Good" bacteria may not respond in a similar manner, and thus may serve as a potential therapeutic approach to engineer the microbiome into a healthier state and treat disease.

[Jo Bowyer]

Count your blessings: Quantitative microbiome profiling

https://www.sciencedaily.com/release...1115131254.htm

A broad range of metabolic and inflammatory diseases is associated with alterations in gut microbiota composition and metabolic potential. Until now, sequencing-based gut microbiota research has been describing such dysbiotic states in terms of proportional shifts in microbiome composition. However, when it comes to the bacterial content of your bowels and how it relates to your health, not only percentages matter, but also numbers count. That is at least one of the main messages of the latest research of Jeroen Raes (VIB-KU Leuven) and his team published in the scientific journal Nature.

In their manuscript entitled 'Quantitative microbiome profiling links gut community variation to microbial load', the VIB-KU Leuven scientists demonstrate a novel methodology that allows both fast and accurate determination of the bacterial load in a fecal sample.

Prof. Jeroen Raes (VIB-KU Leuven): 'The method we developed is based on parallelization of microbiome sequencing and flow cytometry enumeration of microbial cells in fecal material. The combination of these two workflows enables us to generate true quantitative microbiome profiles expressed as numbers of cells per gram, rather than percentages.'

According to the VIB-KU Leuven researchers, Quantitative Microbiome Profiling can really make a difference.

Prof. Jeroen Raes (VIB-KU Leuven): 'Until now, proportional approaches have been the standard in microbiome research. However, without quantitative data, percentages cannot tell you whether a particular bacterium is actually becoming more abundant under specific conditions. A proportional increase could just as well imply that this species of interest is just maintaining is initial levels, while all other taxa are declining. This makes it very difficult to link microbiome data to quantitative health parameters and infer disease mechanisms. With Quantitative Microbiome Profiling, we are one step closer to solving this issue.'

In 2012, Jeroen Raes and his team launched the Flemish Gut Flora Project, one of the first population-level microbiome monitoring efforts worldwide. VIB-VUB-KU Leuven scientists collected over 3000 fecal samples from healthy volunteers. This collection allowed them to assess microbiome variation in a non-diseased population. The results of the Flemish Gut Flora Project proved to be essential for the interpretation of the lab's quantitative microbiome findings.

Prof. Jeroen Raes (VIB-KU Leuven): 'Using the Flemish Gut Flora Project database, we were able to identify a new microbiota community type based on quantitative findings. This enterotype is characterized by a low microbial load. It harbors lower abundances of taxa that might play a role in maintaining a healthy gut ecosystem. While we do observe this enterotype to be present in a minority of healthy volunteers, it is by far the most prevalent microbiota configuration among Crohn's Disease patients.'

Prof. Séverine Vermeire, gastroenterologist at UZ Leuven/KU Leuven: 'Using Quantitative Microbiome Profiling, we observed that feces from Crohn's Disease patients harbor up to 50 times less bacteria than those of healthy volunteers. This striking decrease in bacterial abundance appears to be a key element of dysbiosis in Crohn's Disease. Next steps will be to find out whether having a low cell count enterotype increases your risk of developing Crohn's Disease -- and if so, what can be done to prevent it.'

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[Jo Bowyer]

Age and Gut Bacteria Contribute to Multiple Sclerosis Progression

http://neurosciencenews.com/age-micr...clerosis-7981/

Researchers at Rutgers Robert Wood Johnson Medical School published a study suggesting that gut bacteria at young age can contribute to Multiple sclerosis (MS) disease onset and progression.

[Jo Bowyer]

Bacteria as pacemaker for the intestine

https://www.sciencedaily.com/release...1122103549.htm

[Jo Bowyer]

Traumatic Brain Injury Causes Intestinal Damage

http://neurosciencenews.com/tbi-intestines-8137/

It is not clear how TBI causes these gut changes. A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don’t know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

[Jo Bowyer]

PATIENTS WANT POOP TRANSPLANTS. HERE'S HOW TO MAKE THEM SAFE

https://www.wired.com/story/patients...daily_list1_p4

They're not new, Hitler had one.

POOPDOCTOR.jpg

Just wanted an excuse to get this fabulous version of my favourite emoticon on SS.

[Jo Bowyer]

Tracking effects of a food preservative on the gut microbiome

https://www.sciencedaily.com/release...1218090930.htm

[Jo Bowyer]

New insights into how our bodies maintain a beneficial relationship with our gut microbes

https://www.sciencedaily.com/release...1219092752.htm