Fungus is key factor to Crohn's disease

[jfh]

A Case Western Reserve University School of Medicine-led team of international researchers has for the first time identified a fungus as a key factor in the development of Crohn's disease. The researchers also linked a new bacterium to the previous bacteria associated with Crohn's. The groundbreaking findings, published on September 20th in mBio, could lead to potential new treatments and ultimately, cures for the debilitating inflammatory bowel disease, which causes severe abdominal pain, diarrhea, weight loss, and fatigue.

"We already know that bacteria, in addition to genetic and dietary factors, play a major role in causing Crohn's disease," said the study's senior and corresponding author, Mahmoud A Ghannoum, PhD, professor and director of the Center for Medical Mycology at Case Western Reserve and University Hospitals Cleveland Medical Center "Essentially, patients with Crohn's have abnormal immune responses to these bacteria, which inhabit the intestines of all people. While most researchers focus their investigations on these bacteria, few have examined the role of fungi, which are also present in everyone's intestines. Our study adds significant new information to understanding why some people develop Crohn's disease. Equally important, it can result in a new generation of treatments, including medications and probiotics, which hold the potential for making qualitative and quantitative differences in the lives of people suffering from Crohn's."

Both bacteria and fungi are microorganisms -- infinitesimal forms of life that can only be seen with a microscope. Fungi are eukaryotes: organism whose cells contain a nucleus; they are closer to humans than bacteria, which are prokaryotes: single-celled forms of life with no nucleus. Collectively, the fungal community that inhabits the human body is known as the mycobiome, while the bacteria are called the bacteriome. (Fungi and bacteria are present throughout the body; previously Ghannoum had found that people harbor between nine and 23 fungal species in their mouths.)

The researchers assessed the mycobiome and bacteriome of patients with Crohn's disease and their Crohn's-free first degree relatives in nine families in northern France and Belgium, and in Crohn's-free individuals from four families living in the same geographic area. Specifically, they analyzed fecal samples of 20 Crohn's and 28 Crohn's-free patients from nine families and of 21 Crohn's-free patients of four families. The researchers found strong fungal-bacterial interactions in those with Crohn's disease: two bacteria (Escherichia coli and Serratia marcescens) and one fungus (Candida tropicalis) moved in lock step. The presence of all three in the sick family members was significantly higher compared to their healthy relatives, suggesting that the bacteria and fungus interact in the intestines. Additionally, test-tube research by the Ghannoum-led team found that the three work together (with the E. coli cells fusing to the fungal cells and S. marcescens forming a bridge connecting the microbes) to produce a biofilm -- a thin, slimy layer of microorganisms found in the body that adheres to, among other sites, a portion of the intestines -- which can prompt inflammation that results in the symptoms of Crohn's disease.

This is first time any fungus has been linked to Crohn's in humans; previously it was only found in mice with the disease. The study is also the first to include S. marcescens in the Crohn's-linked bacteriome. Additionally, the researchers found that the presence of beneficial bacteria was significantly lower in the Crohn's patients, corroborating previous research findings.

"Among hundreds of bacterial and fungal species inhabiting the intestines, it is telling that the three we identified were so highly correlated in Crohn's patients," said Ghannoum. "Furthermore, we found strong similarities in what may be called the 'gut profiles' of the Crohn's-affected families, which were strikingly different from the Crohn's-free families. We have to be careful, though, and not solely attribute Crohn's disease to the bacterial and fungal makeups of our intestines. For example, we know that family members also share diet and environment to significant degrees. Further research is needed to be even more specific in identifying precipitators and contributors of Crohn's."


Story Source:
Materials provided by Case Western Reserve University. Note: Content may be edited for style and length.

Journal Reference:
G. Hoarau, P. K. Mukherjee, C. Gower-Rousseau, C. Hager, J. Chandra, M. A. Retuerto, C. Neut, S. Vermeire, J. Clemente, J. F. Colombel, H. Fujioka, D. Poulain, B. Sendid and M. A. Ghannoum. Bacteriome and Mycobiome Interactions Underscore Microbial Dysbiosis in Familial Crohn’s Disease. mBio, September 2016 DOI: 10.1128/mBio.01250-16

 

[D Bergy]

I have a special interest on Crohn's disease since I have done battle with it the past few years. I look at all the research and anecdotal accounts of the disease.

This is likely important to some sufferers of the disease. Given my personal experience with the disease, and other accounts also, I don't believe there is any one pathogen responsible for the symptoms and intestinal inflammation that falls under the Crohn's umbrella.

If you follow the years of research and anecdotal accounts of possible causes, there is a wide range of suspects involved. Two of the most common from condensing all the above appear to be AIEC and Mycobacterium Tuberculosis subspecies Avium aka (MAP)

The study above also indicates E-Coli involvement.

The E-Coli is fairly easily addressed through the use of MMS.

The only practical way I have found to reduce MAP is using a Rife machine and the specific frequencies that damage the pathogen.

Medications really never helped me much. It was not until I discovered at least a majority of the pathogens involved in my disease and a method to reduce them, that my health improved substantially.

To date, this is a list of what causes my symptoms. Possibly through an immune dysfunction aspect of one or more of these, it could be even curative, but at this time I have no evidence that is the case. Currently, I am successfully able to reduce or eliminate the pathogens causing the bulk of my symptoms which are intestinal inflammation and destruction.

Pathogens involved:

MAP
E-Coli. Probably an AIEC variety.
H-Pylori and lots of it.
Mycoplasma pneumonia.
Possibly Klebsiella pneumonia. I have it but so far treating it has only resulted in an eruption of palmoplanter psoriasis. Treatment using the Rife machine may not be as effective as for other pathogens. Still working on that problem.

This is not to say everyone's Crohn's consists of the same pathogens, but it would stand to reason that one or more of these are involved in many cases.

Thanks for the post on the biofilm. Going to do some additional things to see if it is something I need to address.

Dan

 

[jfh]

Thanks for sharing, D Bergy. When I posted this, I was thinking of you. You've obviously researched this considerably. So, I thought a little more info could not hurt. I'm impressed by your research.

 

[D Bergy]

I appreciate it. The research gives me additional things to test, if possible. All the things I treat for now are in a research papers connected to Crohn's or anecdotal information.

Dan

 

[Ted_Hutchinson]

In order to change gut bacterial microbiota (bacteriome) and fungal community (mycobiome,) we have to understand the role of vitamin D3 and anti-microbial antifungal peptides.
Our ability to produce natural antibacterial antifungal peptides in the cathelicidin family depends on the availability of freely bioavailable cholecalciferol.
Because cholecalciferol has a half life of just 24 hrs it's necessary to absorb it (from supplements) or create it DAILY
Because cholecalciferol, vitamin D3 is used by every cell in the body and naturally our skin is set to flood the body with 10,000-20,000iu daily given the chance of full-body UVB exposure, the amounts available in most vitamin D3 supplements are less than the body requires and available cholecalciferol is quickly bound to Vitamin D receptors or vitamin D binding protein therefore the availability of free unbound bioavailable cholecalciferol is limited.
We can measure significant amounts of free vitamin D3 at 50ng/ml 125nmol/l and above maintaining optimal vitamin D status enables a natural regulation of pathogenic bacteria and fungi.
Therefore if we want to maximize our ability to deal with pathogenic bacteria and fungi naturally we need the vitamin d3 status equal to that found in indigenous peoples living traditional lives. 50ng/ml 125nmol/l achieved through DAILY UVB exposure or Vitamin D3 supplement use.
Effects of high doses of vitamin D3 on mucosa-associated gut microbiome

I should have pointed out that because the digestive tracts of Crohn's patients are usually in a wrecked state absorption of vitamin d through the digestive tract may be poor. Apart from UVB exposure, vitamin d3 is well absorbed through the skin so a topical application of drops or cream containing cholecalciferol is well absorbed and tolerated. Sprays that are absorbed through the tissues in the oral cavity are also probably a viable option.
If you've got a stock of vitamin D3 softgels you can snip the ends of the cover and massage the contents into the skin or chewing the softgels and hold the olive oil carrying the cholecalciferol in your mouth for a while would also enable uptake through the tissue under the tongue.

 

[D Bergy]

You are correct that the inflamed intestinal tract absorbs very little of anything. At this time, I am in good shape so that is not currently a problem.

I have been supplementing D3 among other things and get tested at least once a year but usually more often. My last test was 80 which is right about where I want it. A few years ago my initial D level was 15.
It was difficult to get it up to where it is now and it took 25000 to 30000 iu just to get it to start moving up.

While I am able to control my symptoms by removing the pathogens causing them, I am hoping to get my immune system to handle this normally. Not sure if the higher level of D will do that, but there really is no downside in trying. Something is not right with my immune system but with all the possibilities, it is difficult to nail down specifically what the cause is and whether it is correctable.

All in all, I am happy to be back in good health and the long term strategy is as your post suggests, is to get the guts balanced with healthy bacteria while eliminating the bad stuff.

Currently testing out black seed oil to see if killing some yeast does anything. I don't really have any indication that I have excessive yeast but we learn by doing and testing.

Thanks for the link. I wasn't aware that the D influence on the gut microflora was quite that direct.

Dan