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Butyrate producing clostridium probiotics??

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Posted 6/25/2014 4:58 PM (GMT 0)
Here OM/others

I've been looking high and low over the last few days for a probiotic source and or information on probiotics containing both protective (or non-harmful), carbohydrate metabolizing and butyrate producing clostridium bacteria or studies on these and the effects of administration on IBD.

Mainly because all fecal sample studies in IBD show a huge loss in these types of bacteria.

Effect of Clostridium butyricum on fecal flora in Helicobacter pylori eradication therapy
www.wjgnet.com/1007-9327/11/7520.pdf

It's not IBD - but along the lines of what I am looking for.

Fecal Transplant is one way obviously... but I was curious what products/other studies have looked at the combined effects of administering these would be. I finally came across the above a moment ago.

Been thinking about the FT side of of things again - why some get worse like banana, one thing dawned on me - part of the problem may in fact reside in the mast cell/allergy type reaction in these people. The donors may contain a food source antigens that trigger the allergic/innate mast cell degranulation response. The resulting inflammation (increased oxygen) from the response would just kill off the beneficial bacteria again.

Anyway - anyone else have any info of Clostridium containing probiotics?

Post Edited (Canada Mark) : 6/25/2014 11:34:42 AM (GMT-6)

Posted 6/25/2014 5:17 PM (GMT 0)
Down this same road....

A Single Strain of Clostridium butyricum Induces Intestinal IL-10-Producing Macrophages to Suppress Acute Experimental Colitis in Mice:

www.sciencedirect.com/science/article/pii/S1931312813001960
Posted 6/25/2014 5:22 PM (GMT 0)
This is what we all seem to be missing:

Induction of Colonic Regulatory T Cells by Indigenous Clostridium Species:
www.ncbi.nlm.nih.gov/pmc/articles/PMC3969237/
Posted 6/25/2014 5:24 PM (GMT 0)
Mark: You might want to reread this stuff from January.

It is quite interesting that in Vietnam they seem to wipe out their gut bacteria on a routine basis,yet I believe

incidence of IBD to be low.

Stuff I posted the other day,indicates that some antibiotics thin mucus, also butyrate thins mucus..

Really wish I could find dss mouse studies on pesticides,might answer my question as to why

the mice get better.

It seems that in Vietnam they routinely wipe out their gut bacteria with antibiotics. Yet

I do not believe the IBD incidence is high,but not sure.

http://gapsdiet.com/uploads/Newsletter3.pdf

Safety:

http://www.probiotic.org/bacillus-subtilis.htm

http://www.essentialformulas.com/news/Nan_Fuchs_September_Newslet.pdf

http://www.sporegen.com/bacilluspro.html

A heck here is the whole old thread.

https://www.healingwell.com/community/default.aspx?f=38&m=2834542&p=4

Post Edited (Old Mike) : 6/25/2014 11:34:01 AM (GMT-6)

Posted 6/25/2014 6:12 PM (GMT 0)
@ OM - Totally off topic, but are you asking why mice get better after DSS treatment?
Posted 6/25/2014 6:24 PM (GMT 0)
This got me thinking:

There is the lady in the US that did the study on Clostridium species possibly inhabiting (and protecting) the crypts in our colons.... she found this in mice and was moving onto people to see if there's the same effect, since it was normally assumed these areas are bacteria free. She used confocal microscopy to visualize and detect these. More so she suggested the presence of these protect us from certain peptides released during fermentation - which we now know that some bacterial byproducts from gliadin metabolism by microbes (fragilis with certain genes) cause a dramatic immune response. Her work was prior to this and she suggested that these clostridium are present and protective of these byproduct and at the same time provide an energy source for us.

This got me thinking about the effect of not only antibiotics, which seem to full on destroy clostridium type species and lead to a dramatic increase in enterobacteriaceae but also there have been a lot of posts on pesticide and fertilizer again recently.

My question was could these actually interfere or prevent clostridium species from being able to produce spores which might translate to a reduced abundance of these in or normal mucosal flora through lack of exposure. So could Western farming practices reduce protective bacteria basically?

My search was on the effects of Nitrates on Clostridium Sporulation and I came up with this so far:

ACTIVITY OF THREE DISINFECTANTS AND ACIDIFIED NITRITE AGAINST CLOSTRIDIUM DIFFICILE SPORES:
lup.lub.lu.se/luur/download?func=downloadFile&recordOId=118130&fileOId=623878

Though the intention of this if for disinfection of infectious Clostridium Spores, it really would't be a far leap to see how this very process (Nitrate fertilization with the addition of ammonia etc) could prevent/decrease soil sporulation in nature...

Anyway - what happens in nature is the very same thing as in IBD - Excessive application of ammonium nitrate (which is acidified nitrate); when this is applied to soil and left aside and isolated for a year the bacteria balance shifts to very high contents of enterobacteriaceae... same as IBD.

Post Edited (Canada Mark) : 6/25/2014 12:29:45 PM (GMT-6)

Posted 6/25/2014 6:47 PM (GMT 0)
Mararuder: Yes I ask that a few times a month,why after a total disruption of the poor
mice or rat guts,if they stop the DSS the mice usually get better,that is WT mice,of course if knockout they will stay sick.
I also notice that most everything they try on mice, somehow lessens colitis symptoms,perhaps they should look more into what makes it worse.

Here is the latest one.

http://www.ncbi.nlm.nih.gov/pubmed/24236761
Somewhere on here I have a post why DSS or other disrupting chemicals perhaps not the best
approach.
Mark I have huge threads on nitrates/nitrites/fertilizers,timelines somewhat fit,and lest we

forget all the NO leading to facultative bacteria overgrowth,also nitrates converted to nitrite with

our nitrate reducing bacteria in our tongue crypts,swallowed and converted to NO,one of our first

lines of defense.
Old Mike

I posted this stuff last week no one seemed to notice,these bacteria are transmissible to WT mice,

causing disease.

Anyone have increased Prevotellaceae and members of the TM7 phylum, in there gut microbiome testing.

To boot the disease is transferable to WT mice with cohabitation.

Something that was off my radar.  With all the many defense mechanisms in the body,how the hell do we get UC. I know a few here only ate organic prior to UC,also know there are few children who only ate organic and got UC. Something is disrupting perhaps our immune system/gut bacteria in a major way.

http://www.sabiosciences.com/pathwaymagazine/minireview/inflammasome.php

http://www.sciencedirect.com/science/article/pii/S0092867411004806

http://www.ncbi.nlm.nih.gov/pubmed/24581500

Post Edited (Old Mike) : 6/25/2014 1:55:23 PM (GMT-6)

Posted 6/25/2014 8:54 PM (GMT 0)

Old Mike said...
Mararuder: Yes I ask that a few times a month,why after a total disruption of the poor
mice or rat guts,if they stop the DSS the mice usually get better,that is WT mice,of course if knockout they will stay sick.
I also notice that most everything they try on mice, somehow lessens colitis symptoms,perhaps they should look more into what makes it worse.Here is the latest one.
http://www.ncbi.nlm.nih.gov/pubmed/24236761
Somewhere on here I have a post why DSS or other disrupting chemicals perhaps not the best
approach.

You might find this paper/review particularly interesting if you havent already come across it: http://www.ncbi.nlm.nih.gov/pubmed/24250223

You have to remember (which Im sure you already know) that when we are comparing DSS-induced colitis to UC, we are really comparing apples to oranges. While DSS-induced colitis resembles the inflammatory profile of UC the closest (though not perfectly), the etiology of the inflammation is not the same, so the pathogenesis is not the same either. So, for arguments sake, say in humans, the cause of UC is a specific dysbiosis, we wouldnt ever figure that out from a DSS-induced model of colitis.

One small side note, we actually can induce a more chronic DSS-induced colitis through a slight modification to the typical protocol. Im not 100% sure off the top of my head if this is a permanent characteristic, but if i remember correctly it is
Posted 6/25/2014 9:05 PM (GMT 0)
Old Mike, some claim genetic based specific immunodeficiencies cause leaky gut and dysbiosis, especially in crohn's. What are your opinions regarding this idea?
Posted 6/25/2014 9:28 PM (GMT 0)

xy123 said...
Old Mike, some claim genetic based specific immunodeficiencies cause leaky gut and dysbiosis, especially in crohn's. What are your opinions regarding this idea?

Im not OM, but I can put my 2 cents in. Its pretty clear that there is at least some genetic component to the disease; roughly 20% of people with UC have a relative with UC. As for what it affects, leaky gut and dysbiosis are pretty large yet vague concepts, so the genetic based immunodeficiencies likely affect these two areas somewhat at least
Posted 6/25/2014 9:50 PM (GMT 0)
While animal models are of course necessary,as you say they do not tell the whole story.

Never the less,there is a complete disruption of the mucus barrier,yet the mice heal,when DSS is stopped.

But if they use different gene knockout mice,the of course stay sick and die.

xy123: Most probably a genetic component,or epigenetic.

Then again the incidence is increasing as countries westernize,perhaps so there is also a strong

environmental component,some toxin added,or perhaps something missing that was protective.

Certain bacteria,worms.

My son lost his colon,and I have UC.

I am also still not 100% sure it is not transmissible.

Been studying the disease since 1980,and of course I have found no solution.

Hundreds if not thousands of some of the best doc's in the world have been trying to solve it since around,

1900 give or take. 

Will keep at it.

Old Mike

 

Posted 6/26/2014 7:21 AM (GMT 0)
@maurader - DDS colitis is very similar... not apples to oranges at all.

The induction method - loss of barrier function = Colitis in mice as OM points out.

That's #1 to remember with that one in regards to UC. Forget about the inflammatory response that follows. That part just extends current molecular knowledge on inflammatory response.


@OM Maybe it's time to see what's new with the 10,000 biopsy folks as it's been a few years. Many have cited them now. They must have made some progress I'd think. Either that or they hit a dead end. Might be worth an email.


Doesn't answer much but at least it paediatric and prior to any treatment. Been posted before. www.ncbi.nlm.nih.gov/pubmed/24629344 also ties into the clostridia thing.

I had a question for you - but now I forget what it was! Was about paediatric IBD... I'll write when it comes to me again

Post Edited (Canada Mark) : 6/26/2014 1:24:10 AM (GMT-6)

Posted 6/26/2014 11:34 AM (GMT 0)
I have posted this before,but looking for things that make mouse colitis worse,this is one of them.

This statement is also of interest,if true.

"In the past 10 years, genetic research in IBD has been particularly fruitful. However, among the many susceptibility genes identified (>100 to date) none were demonstrated to be necessary or sufficient for disease onset.<!--bib2-->2, <!--bib3-->3"

Old Mike

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998638/

a few more

http://www.ncbi.nlm.nih.gov/pubmed/22235058

I might make mention if you use a coffee maker,at home it might have aluminum components in the

bubble pump,not to mention any pots and pans you might have.

read this old stuff,if it comes up with just page 17,just hit x out where it says clear search

link

Post Edited (Old Mike) : 6/26/2014 6:12:50 AM (GMT-6)

Posted 6/26/2014 1:43 PM (GMT 0)

Canada Mark said...
@maurader - DDS colitis is very similar... not apples to oranges at all.

The induction method - loss of barrier function = Colitis in mice as OM points out.

That's #1 to remember with that one in regards to UC. Forget about the inflammatory response that follows. That part just extends current molecular knowledge on inflammatory response.

Yes but my point is that it completely disregards large components involved in the pathogenesis of the disease (i.e. the role of the immune system, autoantibodies, genetic components, etc). So while the inflammatory profile may be fairly similar, we are missing far too much for it to be an ideal model.

There is a reason we have so many different models of colitis, because they all address different components. Check out the images in the link I posted above, thatll make clear what Im referring to
Posted 6/27/2014 12:18 AM (GMT 0)
That's making the bold assumption that the immune system is the actual "cause"... That's the unknown. pathogenesis = direct cause.

What works best or the closest ideal model so far is actually DDS. At the moment it supports all of the direct visual investigations (Microscopy) of human biopsy samples and disease progression.

------

OM - It just came to me the question I had for you. Have you come across any paediatric studies on colonic mucus in general? Like mucus layer development over time? Sulfur/salio components etc. Have you ever come across anything like that - perhaps with mucosal bacterial samples in comparison to adults as well. Just curious on some stuff but had some trouble digging it out. Same with say paediatric incidence increase over time - like how many young children are now coming down with IBD compared to say 10 or 20 years ago.
I guess we know what the bacterial makeup is already in children with IBD though. Same as adults basically.

In a nutshell I think I'm looking for how the mucosal system develops over time. Is there always a thick and loose layer etc, that type of thing.
Posted 6/27/2014 12:28 AM (GMT 0)

Canada Mark said...
That's making the bold assumption that the immune system is the actual "cause"... That's the unknown. pathogenesis = direct cause.

What works best or the closest ideal model so far is actually DDS. At the moment it supports all of the direct visual investigations (Microscopy) of human biopsy samples and disease progression.
.

But we do know that there is an immune component, as well as genetic component, etc. So disregarding them is just as bold an assumption. The DSS model is best for investigating some aspects of UC, but certainly not all; thats why we have so many other models.
Posted 6/27/2014 12:53 AM (GMT 0)
Posted about this awhile back but Biflac is the best, its hard to get your hands on since you have to get someone in india to send it to you. I took it just for grins and giggles.... and have a friend with UC on it that is getting some great results.

www.abpl.co.in/images/biflac.pdf
Posted 6/27/2014 11:48 AM (GMT 0)
Mark: This new news says huge increase of crohns in England over the past few years.

These numbers if true are real real scary, sucralose anyone.

This kink of increase just doesn't happen by itself.

http://www.bbc.co.uk/newsbeat/27810066

Don't think I remember anything on pediatric mucus thickness,but may just not remember.

While looking around I did find this stuff which thins the colon mucus and messes with gut bugs.

Lubiprostone decreases mouse colonic inner mucus layer thickness and alters intestinal microbiota

http://www.ncbi.nlm.nih.gov/pubmed/23329012

Old Mike

 

Post Edited (Old Mike) : 6/27/2014 6:43:48 AM (GMT-6)

Posted 6/27/2014 5:13 PM (GMT 0)
I think a big part of the problem is every day that goes by there are more and more gene mutations passed on. At the same time we have figured out how to live longer we are getting sicklier and sicklier. Are those things caused by environmental factors such as antibacterial items, antibiotics, more chemicals, western diets, etc., or is much of this really due to more and more gene mutations? Is it possible that if the human race survives another 100,000 years that everyone born will have multiple gene mutations to deal with, no matter what lifestyle we lead? Of course it's probably a combination of all of the above but it makes you think what the human race will be like far in to the future. Maybe due to genetics alone we are all doomed.
Posted 6/27/2014 6:20 PM (GMT 0)
Maybe over time when mutations and gene activation are further understood some answers will flush out. A lot is still very poorly understood. On the plus side there's been some amazing progress lately. Especially with being able to repair gene that is causing a known problem - using bacteria in mice. Now they are trying to see if it will work in humans eventually. But of course, one needs to know exactly what is causing the problem in the first place.

So in the mice let's say they had a gene where there was a C (Cytosine) instead of a G (Guanine) somewhere within the coding and this causes a specific known problem - they use the bacteria (I don't exactly know how) but they can then go in a replace the C with the G again and as the cells replicate the genetic problem disappears and the mice get better.

It's really pretty darn amazing.

Does make you wonder though. Imagerdner pointed out something similar to you recently. I forget what was said but something along the lines of those that can survive and thrive junk food, chemicals etc are the one's who will thrive - so maybe in the future everyone will eat chips and pop and weigh a ton sort of thing. However it was worded it was pretty funny.

@OM

Wat about anal bacteria? and/or anal mucus (if there is any)... going back the UC starts distally sort of thing. I haven't found many studies on anal bacteria and mucus.... doesn't seem like the type of topic most grad students would be interested in :)

Just thinking about the distal thing, combined with partial colectomy where when they try attaching back to the anus the remaining healthy colon section develops UC...

Also in FT where they only place a small about via quick enema for 30 seconds or so as the bacteria move upwards (according to some GI's).

Maybe it's something as simple as scratching your but without washing your hands first! Transmission of something takes place type thing.
Posted 6/27/2014 9:27 PM (GMT 0)
I think I am going to keep quoting this.

"In the past 10 years, genetic research in IBD has been particularly fruitful. However, among the many susceptibility genes identified (>100 to date) none were demonstrated to be necessary or sufficient for disease onset.

 

If you read my thread on how I think I got UC,I had none IBD related anal,fistulas/fissures/abcesses for 8 years prior to getting UC.

The old fart proctologist who used to stick a rigid sig scope into me once a month thought that the bacteria from all the abscesses caused the UC.

 

I can see where this might happen,and I am still not 100% that UC is not contagious.

Again with how sophisticated our immune system is, something really really has to be going wrong,for us to get sick.

Old Mike

 

 

Post Edited (Old Mike) : 6/29/2014 6:46:22 AM (GMT-6)

Posted 6/27/2014 10:09 PM (GMT 0)
Sweet find path...

I'd be interested in looking into this. Thanks
Posted 6/28/2014 4:41 PM (GMT 0)

garylouisville said...
I think a big part of the problem is every day that goes by there are more and more gene mutations passed on. At the same time we have figured out how to live longer we are getting sicklier and sicklier. Are those things caused by environmental factors such as antibacterial items, antibiotics, more chemicals, western diets, etc., or is much of this really due to more and more gene mutations? Is it possible that if the human race survives another 100,000 years that everyone born will have multiple gene mutations to deal with, no matter what lifestyle we lead? Of course it's probably a combination of all of the above but it makes you think what the human race will be like far in to the future. Maybe due to genetics alone we are all doomed.


We arent doomed. But we cannot go on living the way we do. We innundate our bodies with so much crap that it has to process and our genes are "weaker" or in some ways the SNP isnt a weakness, its an adaptation so that our bodies can try and compensate for these new things. We are drowning in toxins. And that is why when a stealth pathogen gets a foot hold we get chronic disease.. we used to have stronger immune capabilities, but in order to live in this world where we are getting innundated with all of this crap every minute our immune system has had to adapt.

Chemicals, gmos, plastics.. these are the plagues of our times and if we cant find a better balance with the earth and environment, it's about to spank our collective asses basically.

Ive been travelling and relaxing a lot lately.. but have you looked at the people around you lately? I didnt used to notice.. but man, people are not looking good. They are fat and pasty.. we dont know how to talk to each other.. we carry around our own little cell phone ***ushima... the things we eat.. wow.. I went to the fair last night, that is all I can say about that. Beyond just that... everyone is sick.. everyone is taking something for something.

I actually think well used antibiotics are one of the best tools we have but they can also be one of our worst enemies too.
Posted 6/28/2014 4:44 PM (GMT 0)

Old Mike said...

I can see where this might happen,and I am still not 100% that UC is not contagious.
Again with how sophisticated our immune system is, something really really has to be going wrong,for us to get sick.
Old Mike



Well, good.. cause UC is caused by a pathogen (but that pathogen is NOT the same for everyone) and weak spots in your personal epigenetic code. Im glad you are starting to come around. ;)

Our immune systems only break when they have been fighting something so long without help that they have no other choice.. and even then.. even then.. we can bring them back online because the human body is amazing when it has the things it needs.
Posted 6/29/2014 12:41 PM (GMT 0)
Canada...where did you read about using bacteria to modify genes? Could this same process have been used by a pathogen to give me colitis in the first place?

If this disease is genetic...was I in remission for 24 years before contracting it? Or did my genes change?
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